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EEG Atlas: EEG Artifacts

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EEG Atlas: Encephalopathic Patterns I - Generalized Slowing

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EEG Atlas: Encephalopathic Patterns II - More Severe Patterns

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EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns

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EEG Atlas: Epileptiform Normal Variants

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EEG Atlas: Focal (Nonepileptic) Abnormalities

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EEG Atlas: Generalized Epilepsies

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EEG Atlas: Localization-related Epilepsies

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EEG Atlas: Normal Awake EEG

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EEG Atlas: Normal Sleep EEG - Rapid Eye Movement Sleep

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EEG Atlas: Normal Sleep EEG - Stage I

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EEG Atlas: Normal Sleep EEG - Stage II

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EEG Atlas: Normal Sleep EEG - Stages III and IV

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eMedicine - EEG Atlas: EEG Artifacts : Article by Selim R Benbadis, MD

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EEG Atlas: EEG Artifacts

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Last Updated: May 30, 2002

AUTHOR INFORMATION

Section 1 of 6

Author Information Introduction Physiologic Artifacts Extraphysiologic Artifacts Pictures Bibliography

Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Paul E Barkhaus, MD, Director, Division of Neuromuscular Diseases, Milwaukee Veterans Administration Medical Center; Professor, Department of Neurology, Medical College of Wisconsin; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

Section 2 of 6


Although EEG is designed to record cerebral activity, it also records electrical activities arising from sites other than the brain. The recorded activity that is not of cerebral origin is termed artifact and can be divided into physiologic and extraphysiologic artifacts. While physiologic artifacts are generated from the patient, they arise from sources other than the brain (ie, body). Extraphysiologic artifacts arise from outside the body (ie, equipment, environment). PHYSIOLOGIC ARTIFACTS

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Muscle (electromyogram) activity Myogenic potentials are the most common artifacts (see Images 1-2). Frontalis and temporalis muscles (eg, clenching of jaw muscles) are common causes. As a general rule, the potentials generated in the muscles are of

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shorter duration than those generated in the brain and are identified easily on the basis of duration, morphology, and rate of firing (ie, frequency). Particular patterns of electromyogram (EMG) artifacts can occur in some movement disorders. Essential tremor and Parkinson disease can produce rhythmic 4- to 6-Hz sinusoidal artifacts that may mimic cerebral activity. Another disorder that can produce repetitive muscle artifacts is hemifacial spasm. The photomyoclonic response is a special type of EMG artifact that occurs during intermittent photic stimulation. Some subjects contract the frontalis and orbicularis muscles. These contractions occur approximately 50-60 milliseconds after each flash, disappear after eye opening and use of paralyzers, are located mostly frontally, and have no concomitant EEG changes. Glossokinetic artifact In addition to muscle activity, the tongue (like the eyeball) functions as a dipole, with the tip negative with respect to the base. In this case the tip of the tongue is the most important part because it is more mobile. The artifact produced by the tongue has a broad potential field that drops from frontal to occipital areas, although it is less steep than that produced by eye movement artifacts. The amplitude of the potentials is greater inferiorly than in parasagittal regions; the frequency is variable but usually in the delta range and occurs synchronously when the patient says “Lah-lah-lah-lah” or “Lilt-lilt-lilt-lilt,” which can be verified by the technologist. Chewing and sucking can produce similar artifacts. These commonly are observed in young patients. However, they also can be observed in patients with dementia or those who are uncooperative. Eye movements Eye movements are observed on all EEGs and are useful in identifying sleep stages. The eyeball acts as a dipole with a positive pole oriented anteriorly (cornea) and a negative pole oriented posteriorly (retina). When the globe rotates about its axis, it generates a large-amplitude alternate current field, which is detectable by any electrodes near the eye. The other source of artifacts comes from EMG potentials from muscles in and around the orbit. Vertical eye movements typically are observed with blinks (ie, Bell phenomenon). A blink causes the positive pole (ie, cornea) to move closer to frontopolar (Fp1-Fp2) electrodes, producing symmetric downward deflections. During downward eye movement the positive pole (ie, cornea) of the globe moves away from frontopolar electrodes, producing an upward deflection best recorded in channels 1 and 5 in the bipolar longitudinal montage. Lateral eye movements most affect lateral frontal electrodes F7 and F8 (see Images 3-4). During a left lateral eye movement, the positive pole of the globe moves toward F7 and away from F8. Using a bipolar longitudinal montage, maximum positivity in electrode F7 and maximum negativity in electrode F8 is recorded, and artifacts do not occur in channels 9 and 13 or 10 and 14. A so-called rectus lateralis may be present in electrode F7; it is observed best in the vertex reference montage. With right lateral eye movement, the opposite occurs. ECG artifact Some individual variations in the amount and persistence of ECG artifact are related to the field of the heart potentials over the surface of the scalp. Generally, people with short and wide necks have the largest ECG artifacts on their EEGs. The voltage and apparent surface of the artifact vary from derivation to derivation and, consequently, from montage to montage. The artifact is observed best in referential montages using earlobe electrodes A1 and A2. ECG artifact is recognized easily by its rhythmicity/regularity and coincidence with the ECG tracing (each “sharp wave” equals artifact that synchronizes with each QRS complex of the ECG channel; see Image 5). The situation becomes difficult when cerebral abnormal activity (eg, sharp waves) appears intermixed with EEG artifact, and the former may be overlooked. The EEG technologist should apply electrodes routinely to record the ECG. Pulse Pulse artifact occurs when an EEG electrode is placed over a pulsating vessel. The pulsation can cause slow waves that may simulate EEG activity. A direct relationship exists between ECG and the pulse waves. The QRS complex (ie, electrical component of the heart contraction) happens slightly ahead of the pulse waves (200-300



millisecond delay after ECG equals QRS complex). Respiration artifacts Respiration can produce 2 kinds of artifacts. One type is in the form of slow and rhythmic activity, synchronous with the body movements of respiration and mechanically affecting the impedance of (usually) one electrode. The other type can be slow or sharp waves that occur synchronously with inhalation or exhalation and involve those electrodes on which the patient is lying. Several commercially available devices to monitor respiration can be coupled to the EEG machine. As with the ECG, one channel can be dedicated to respiratory movements. The simplest way to monitor respiration is by the EEG technician making notations with a pencil (ie, upward movement of the pencil for inhalations, downward return for exhalations). Skin artifacts Biological processes and/or defects may alter impedance and cause artifacts. Sweat is a common cause (see Image 6). Sodium chloride and lactic acid from sweating reacting with metals of the electrodes may produce huge slow baseline sways. Significant asymmetry also can be observed when a collection (eg, subgaleal hematoma) is under or in the skin. In this last example, the amplitude of the background rhythm is reduced in derivations from electrodes overlying the hematoma. Skull defects also can be the source of asymmetry. In this situation, amplitudes are greater in derivations from electrodes overlying or adjacent to skull defects. EXTRAPHYSIOLOGIC ARTIFACTS

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Electrodes The most common electrode artifact is the electrode popping. Morphologically this appears as single or multiple sharp waveforms due to abrupt impedance change. It is identified easily by its characteristic appearance (ie, abrupt vertical transient that does not modify the background activity) and its usual distribution, which is limited to a single electrode. In general, sharp transients that occur at a single electrode should be considered artifacts until proven otherwise (see Image 6). At other times, the impedance change is not so abrupt, and the artifact may mimic a low-voltage arrhythmic delta wave (see Images 7-11). Alternating current (60-Hz) artifact Adequate grounding on the patient has almost eliminated this type of artifact from power lines. The problem arises when the impedance of one of the active electrodes becomes significantly large between the electrodes and the ground of the amplifier. In this situation, the ground becomes an active electrode that, depending on its location, produces the 60-Hz artifact (see Image 12). The artifact presents at exact frequency (60 Hz, as its name indicates). A better identification can be made by increasing the paper speed (ie, sweep time) to 60 mm/s and counting it (1 cycle per millimeter). Movements in the environment Movement of other persons around the patient can generate artifacts, usually of capacitive or electrostatic origin. Avoid this type of artifact as much as possible. If avoidance is not possible, as in the ICU and the operating room, place proper notation on the records. Another artifact, probably due to electrostatic changes on the drops, can be introduced by a gravity-fed intravenous infusion. Morphologically this appears as spike transient potentials at fixed intervals that coincide with drops of the infusion. With the increasing use of automatic electric infusion pumps, a new type of artifact, infusion motor artifact (IMA), has arisen. Morphologically, IMA appears as very brief spiky transients, sometimes followed by a slow



component of the same polarity. Its frequency does not relate directly to drop rate. Lininger et al have suggested that this artifact arises from electromagnetic sources. The artifact produced by respirators varies widely in morphology and frequency. Monitoring the ventilator rate in a separate channel helps to identify this type of artifact. Interference from high-frequency radiation from radio, TV, hospital paging systems, and other electronic devices can overload EEG amplifiers. The pens may deflect upward or downward to full excursion, and no EEG can be recorded. The cutting and/or coagulating electrode used in the operating room also generates high-voltage highfrequency signals that interfere with the recording system. The best thing to do is turn off the EEG machine while using this instrument. PICTURES

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Caption: Picture 1. EEG atlas: EEG artifacts. Electromyogram (muscle) artifact best observed in the left temporal region. ECG artifact also is present, best observed in the posterior region.

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eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: EEG artifacts. Electromyogram (muscle) artifact. These waveforms represent motor unit potentials as typically observed on needle electrode examination during electromyogram, with a frequency of 20-100 Hz. Distribution varies, and in this case it is more prominent on the left side. Such artifact can be diminished by the judicious use of the high-frequency filter. (This sample has the default setting of highfrequency filter 70 Hz.)


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: EEG artifacts. Eye movements such as these usually are observed in frontal electrodes and not further posteriorly then the midtemporal region. The phase reversals at lateral frontal electrodes F7 and F8 are of opposite polarity, indicating lateral eye movements. Because the cornea is charged positively and the retina negatively, the side of the positivity indicates the direction of eye movement. Thus, the first one here is to the right.


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Caption: Picture 4. EEG atlas: EEG artifacts. Left frontal artifact in the fourth second. This is not limited to a single electrode and has the morphology of an eye movement, but it is unilateral. This is an eye movement in a patient who has a glass left eye.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 5. Regular (periodic) slow waves best observed at midtemporal and posterior temporal electrodes T4-T6 and T3-T5. These clearly are related to ECG. The duration and morphology are those of pulse artifact, but as demonstrated by the marker, no delay occurs between the ECG and the artifact. Thus this is an ECG artifact with broad QRS complexes.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: EEG artifacts. Sweat artifact. This is characterized by very low-frequency (here, 0.25- to 0.5-Hz) oscillations. The distribution here (midtemporal electrode T3 and occipital electrode O1) suggests sweat on the left side. Note that morphology and frequency are also consistent with slow rolling eye movements, but distribution is not.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 7. EEG atlas: EEG artifacts. Electrode artifact at frontal pole electrode Fp1. The duration is too short ("narrow") for any cerebral potential, and the distribution is limited to a single electrode (Fp1). In general, activity that affects a single electrode (ie, without the expected drop off and activity at neighboring electrodes or "plausible field") should be considered an artifact until proven otherwise.


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Picture Type: Photo Caption: Picture 8. EEG atlas: EEG artifacts. Electrode artifact at occipital electrode O1. The morphology is very unusual for any cerebral waveform, and the distribution is limited to a single electrode. In general, activity that affects a single electrode (ie, without the expected drop off and activity at neighboring electrodes or "plausible field") should be considered an artifact until proven otherwise.




eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 9. EEG atlas: EEG artifacts. Electrode artifact at frontal electrode F3. This should not be misinterpreted as a spike. This sharply contoured transient clearly occurs at only one electrode, as confirmed on the referential montage.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 10. EEG atlas: EEG artifacts. Electrode (impedance) artifact at parietal electrode P3. Initially, a slow artifact is followed by a more abrupt one at the seventh second. This commonly is referred to as an electrode pop. Note again the unusual morphology of the sharp component and that it is at a single electrode. Also note an eye blink in the third second and slight electromyogram artifact in the frontal regions in the first 2 seconds.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 11. EEG atlas: EEG artifacts. Just as electrode artifacts can simulate interictal spikes, they also can mimic an ictal pattern. This rhythmic artifact may be mistaken for an electrographic seizure or subclinical rhythmic epileptiform discharges of adults (SREDA; see Normal EEG Variants). However, this is confined to a single electrode (posterior temporal electrode T6), as can be confirmed on a referential montage. This artifact often is confirmed by the presence of other definite electrode pops in the same electrode.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 12. EEG atlas: EEG artifacts. Ground recording artifact. This is a somewhat less common electrode artifact, also related to accidentally high impedance. The high impedance at posterior temporal electrode T6 results in this electrode recording from the ground on the forehead, thus picking up eye movements (which normally should not be observed at T6).




eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 13. PowerPoint presentation of Images 1-12.

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Bickford RG, Keith HM: Convulsive effects of light stimulation in children. Am J Dis Child 1953; 86: 170-83. Daly D, Pedley T, eds: Current Practice of Clinical Electroencephalography. 2nd ed. New York: Raven Press; 1990. Lininger AW, Volow MR, Gianturco DT: Intravenous infusion motor artifact. Am J EEG Technol 1981 Dec; 21(4): 167-73[Medline]. Luders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000. Picton TW, van Roon P, Armilio ML, et al: The correction of ocular artifacts: a topographic perspective. Clin Neurophysiol 2000 Jan; 111(1): 53-65[Medline]. Redding FK, Wandel V, Nasser C: Intravenous infusion drop artifacts. Electroencephalogr Clin Neurophysiol 1969 Mar; 26(3): 31820[Medline]. Schwab RS, Cobb S: Simultaneous EMG’s and EEG’s in paralysis agitans. J Neurophysiol 1939; 2: 36-41. Shaffer MA: Problem record of the month. No. 3: Asymmetrical eyeblink artifact. Am J EEG Technol 1970; 10: 153-6. Tyner F, Knott J, Mayer Jr W, eds: Fundamentals of EEG technology. In: Basic Concepts and Methods. Vol 1. NY: Raven Press; 1983. van de Velde M, van Erp G, Cluitmans PJ: Detection of muscle artifact in the normal human awake EEG. Electroencephalogr Clin Neurophysiol 1998 Aug; 107(2): 149-58[Medline]. Westmoreland BF, Espinosa RE, Klass DW: Significant prosopoglossopharyngeal movements affecting the EEG. Am J EEG Technol 1973; 13: 59-70. Young GB, Campbell VC: EEG monitoring in the intensive care unit: pitfalls and caveats. J Clin Neurophysiol 1999 Jan; 16(1): 405[Medline].

NOTE: Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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eMedicine - EEG Atlas: Encephalopathic Patterns I - Generalized Slowing : Article by Selim R Benbadis, MD


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Last Updated: June 12, 2002

AUTHOR INFORMATION

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Section 1 of 6

Author Information Introduction Waveform Description Clinical Correlation Pictures Bibliography

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Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

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Since the EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of diffuse brain dysfunction (ie, diffuse encephalopathy). This article discusses generalized slowing, which is the most common finding in diffuse encephalopathies. (Focal [localized] slow activity reflects focal dysfunction, not diffuse dysfunction [ie, encephalopathy].) The next level of severity of diffuse brain dysfunction is discussed in EEG Atlas: Encephalopathic Patterns II - More Severe Patterns, and other encephalopathic patterns are discussed in EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns. Generalized slowing can be divided in a clinically useful way into 3 patterns: background slowing, intermittent slowing, and generalized slowing. WAVEFORM DESCRIPTION

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Background slowing: A posterior dominant and reactive background is present, but its frequency is too slow for the patient’s age. The lower limit of normal generally is considered to be 8 Hz beginning at age 8 years. A guideline to remember the lower limits of normal is as follows: 5-6-7-8 Hz at ages 1-3-5-8 years, respectively (see Images 1-2). Intermittent slowing: This involves bursts of generalized slowing, usually polymorphic delta. More rarely, the intermittent bursts are in the theta frequency range, and occasionally they can be rhythmic rather than polymorphic. When rhythmic, this pattern sometimes is referred to as frontal intermittent rhythmic delta activity (FIRDA). The EEG is still reactive to external stimulation and, for example, may have evidence of state changes such as drowsiness or sleep. A posterior dominant background is usually present, and it may be normal or slow in frequency (see Image 2). Continuous slowing: Polymorphic delta activity (PDA) occupies more than 80% of the record. This is usually unreactive, and a posterior dominant background is usually absent (see Images 3-4).

CLINICAL CORRELATION

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Essentially, the 3 levels of slowing described above represent 3 degrees of severity (ie, mild, moderate, and severe) of diffuse encephalopathy. As usual, this is completely nonspecific as to etiology and most commonly is observed in metabolic and toxic (including medication-induced) encephalopathies. It also can be observed in diffuse structural or degenerative processes. However, most slowly progressive neurodegenerative diseases (eg, dementias of the Alzheimer type) go along with a normal EEG until the very late stages. PICTURES

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Caption: Picture 1. EEG atlas: encephalopathic patterns I – generalized slowing. Background slowing. The posterior dominant background (alpha rhythm) is at 7 Hz, slower than the alpha frequency range. No other generalized slow activity is present. Since this patient is older than 8 years, and is clearly awake, this is abnormal. This represents (electrographically) the mildest degree of diffuse encephalopathy.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: encephalopathic patterns I – generalized slowing. (1) Background slowing and (2) intermittent slowing, generalized. Mild diffuse encephalopathy; a posterior dominant background is present, but it is only at 6-7 Hz, and bursts of generalized polymorphic delta activity (this one lasting 2-3 s) are present.





Caption: Picture 3. EEG atlas: encephalopathic patterns I – generalized slowing. Continuous slowing, generalized. The record is dominated by generalized polymorphic delta activity. When this is "continuous" (greater than 80% of the recording), it usually goes along with a severe diffuse encephalopathy. This is nonspecific in regard to etiology and most commonly is due to metabolic or systemic disturbances.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: encephalopathic patterns I – generalized slowing. Continuous slowing, generalized. While some faster frequencies are present, this sample is dominated by generalized polymorphic delta activity. If this is "continuous" (greater than 80% of the recording), this usually goes along with a severe diffuse encephalopathy.


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Geller E: Generalized disturbances of brain function: encephalopathies, coma, degenerative diseases, and brain death. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders; 2000: 438-455. Levin KH, Lüders HO, eds: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000. Luders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000.


EEG Atlas: Encephalopathic Patterns I - Generalized Slowing excerpt



eMedicine - EEG Atlas: Encephalopathic Patterns II - More Severe Patterns : Article by Selim R Benbadis, MD


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Synonyms and related keywords: brain death, ECI, electrocerebral inactivity, periodic patterns, burstsuppression, periodicity AUTHOR INFORMATION

Section 1 of 6



Section 2 of 6


Since EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of diffuse brain dysfunction (ie, diffuse encephalopathy). Generalized slowing is discussed in EEG Atlas: Encephalopathic Patterns I - Generalized Slowing, and other encephalopathic patterns are discussed in EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns. This article reviews patterns that generally are considered the next level of severity beyond generalized slowing. These patterns include periodic patterns (such as burst-suppression), background suppression, and electrocerebral inactivity (ECI). WAVEFORM DESCRIPTION

Section 3 of 6


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eMedicine - EEG Atlas: Encephalopathic Patterns II - More Severe Patterns : Article by Selim R Benbadis, MD Author Information Introduction Waveform Description Clinical Correlation Pictures Bibliography

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Periodic patterns (Image 1): Discharges occur at regular intervals (ie, periodicity). The discharges are typically complex and multiphasic and often are epileptiform in morphology. Thus they are like periodic lateralizing epileptiform discharges (PLEDs) except that, instead of being lateralized, they are generalized. They sometimes are referred to as generalized periodic epileptiform discharges (GPEDs). Their periodicity rather than their morphology sets them apart as a unique and clinically useful entity (as is true for PLEDs). By contrast, the term bi-PLEDs usually refers to periodic discharges that are bihemispheric but asynchronous (ie, independent). Burst-suppression pattern (Image 2): This subtype of periodic pattern consists of bursts of activity (mixture of sharp and slow waves) periodically interrupted by episodes of suppression (activity <10 µV). Typically, the episodes of suppression are longer (typically 5-10 s) than the bursts of activity (typically 13 s). Background suppression: This is a “nearly flat” EEG, with very low voltage activity (<10 µV) and no reactivity, but the activity is still too large to meet criteria for ECI. Electrocerebral inactivity (Image 3): ECI is defined by no activity greater than 2 µV; to support a diagnosis of brain death while avoiding “overcalling” brain death, ECI must be recorded according to strict guidelines. These requirements specify recording time, double interelectrode distances, testing reactivity, and the integrity of the system. (See Generalized EEG Waveform Abnormalities for the ECI Guidelines of the American Clinical Neurophysiology Society.)


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As usual, these severe encephalopathic patterns are completely nonspecific as to etiology but represent extremely severe degrees of diffuse encephalopathy. Because sedative medications can cause or aggravate these abnormalities, careful interpretation is warranted when reading these patterns. These patterns are indicative of very severe brain dysfunction if sedative medications can be excluded with certainty as their cause. Periodic patterns, including burst-suppression patterns, are somewhat more common in anoxic injuries than in other systemic disturbances. Periodic patterns can be induced by high doses of sedatives such as barbiturates, benzodiazepines, or propofol. In fact, burst-suppression pattern is typically the goal and the method used to titrate doses of anesthetics for treatment of refractory status epilepticus. In the appropriate clinical context, certain periodic patterns can suggest and support the diagnoses of Creutzfeldt-Jakob disease (CJD) and subacute sclerosing panencephalitis (SSPE). Classically, the periodicity for CJD is approximately 1-2 seconds, whereas it is much longer in SSPE (approximately 4-10 s). Rhythmicity or periodicity is one of the hallmarks of electrographic seizures; thus periodic patterns quite often are observed in the context of nonconvulsive status epilepticus. Often the decision whether to consider a periodic pattern ictal must rely on clinical information or the response to anticonvulsant treatment. ECI is supportive of a clinical diagnosis of brain death. Remembering and emphasizing that brain death is a clinical diagnosis is important. Contrary to a common misconception, EEG is not required for the diagnosis of brain death and is considered only as a supportive test.


eMedicine - EEG Atlas: Encephalopathic Patterns II - More Severe Patterns : Article by Selim R Benbadis, MD

PICTURES

Section 5 of 6


Caption: Picture 1. EEG atlas: encephalopathic patterns II – more severe patterns. Classification: periodic pattern, generalized. The periodicity here is approximately 1 second.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: encephalopathic patterns II – more severe patterns. Classification: burstsuppression. Note that this is a 15-second segment, to show the periods of suppression (4-5 s) separated by the bursts. Suppression periods are characterized by activity less than 10 µV.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: encephalopathic patterns II – more severe patterns. Classification: electrocerebral inactivity. The recording demonstrates no cerebral activity greater than 2 µV. Given the high sensitivity (2 µV/mm), a combination of ECG and 60-Hz artifact often is present, as observed here.



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American EEG Society: Guideline three: minimum technical standards for EEG recording in suspected cerebral death. American Electroencephalographic Society. J Clin Neurophysiol 1994 Jan; 11(1): 10-3[Medline]. Geller E: Generalized disturbances of brain function: encephalopathies, coma, degenerative diseases, and brain death. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:438-455. Husain AM, Mebust KA, Radtke RA: Generalized periodic epileptiform discharges: etiologies, relationship to status epilepticus, and prognosis. J Clin Neurophysiol 1999 Jan; 16(1): 51-8[Medline]. Levin KH, Lüders HO, eds: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000. Luders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000.

NOTE:


eMedicine - EEG Atlas: Encephalopathic Patterns II - More Severe Patterns : Article by Selim R Benbadis, MD Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

EEG Atlas: Encephalopathic Patterns II - More Severe Patterns excerpt



eMedicine - EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns : Article by Selim R Benbadis, MD


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Synonyms and related keywords: alpha coma, beta coma, spindle coma, triphasic waves AUTHOR INFORMATION

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Section 1 of 6

Author Information Introduction Waveform Descriptions Clinical Correlation Pictures Bibliography



Continuing Education Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

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Since EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of diffuse brain dysfunction (ie, diffuse encephalopathy). Generalized slowing is discussed in EEG Atlas: Encephalopathic Patterns I - Generalized Slowing, and more severe patterns (ie, periodic patterns, such as burst-suppression, background suppression, and electrocerebral inactivity) are discussed in EEG Atlas: Encephalopathic Patterns II - More Severe Patterns. This article reviews less common encephalopathic patterns, including alpha coma, beta coma, spindle coma, and triphasic waves. WAVEFORM DESCRIPTIONS

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Unusual special patterns observed in comatose patients include alpha coma (Image 1), beta coma (Image 2), and spindle coma (Image 3). ●

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These patterns are characterized by electrical activity that morphologically resembles and sometimes appears nearly identical to normal waveforms (ie, alpha rhythm, beta activity, spindles). To be classified as one of these patterns, the activity should be frankly excessive in amplitude or in spatial distribution (ie, widespread), appear in unusual spatial distribution, or appear excessive in amount (ie, near continuous). Although some investigators classify these patterns as abnormal even if the pattern is reactive, unreactive activity is preferred. The most important criterion is patient coma at the time of clinical recording.

Triphasic waves are frontally positive sharp transients, usually of greater than 70 microvolts amplitude (see Image 4). The positive phase usually is preceded and followed by a smaller negative waveform. As a rule, the first negative wave is of higher amplitude than the second. They are bilateral and occur in bursts of repetitive waves at 1-3 Hz. No reactivity is the rule, and often an anterior-posterior temporal lag can be observed. The largest deflection is usually frontal, and in ear referential montage the time lag is usually not present. The usual clinical correlate of triphasic waves is a metabolic or other diffuse encephalopathy. Thus, a triphasic morphology (while necessary) is not sufficient to classify a record as "triphasic waves." CLINICAL CORRELATION

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Alpha coma, beta coma, and spindle coma are infrequent. They are, like all the encephalopathic patterns, nonspecific in regard to etiology, although anoxia often is associated with alpha coma and drugs with beta coma. They are generally indicative of a severe degree of encephalopathy. Reactivity is a good prognostic factor. In fact, some investigators, including the author, do not classify a record as alpha or spindle coma if it is reactive. Triphasic waves classically are associated with hepatic encephalopathy. However, they are not specific and can be observed in uremic encephalopathy and even other types of metabolic derangements. Many other patterns can have a triphasic morphology. Like periodic patterns, triphasic waves quite often are observed in the context of nonconvulsive status epilepticus. Often the decision whether to consider triphasic waves ictal must rely on the clinical information or the response to anticonvulsant treatment. PICTURES

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Caption: Picture 1. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Alpha coma. Unlike a normal alpha rhythm, the alpha activity observed here is not posterior dominant, is continuous, and is nonreactive. If the entire record is present and the patient is known to be comatose, this qualifies as alpha coma.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Beta coma. Prominent fast (beta) activity is noted at 15-22 Hz. To qualify as "excessive fast" activity, the pattern has to be the predominant frequency and excessive in amount (ie, nearly continuous and unreactive) and amplitude, ie, greater than the typical 30 microvolts of the normal beta activity. Note that this pattern could be seen in an awake patient, so that the term "beta coma" is reserved for patients known to be comatose.




eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Spindle coma. Note the prominent spindlelike activity at 13-16 Hz. Typically, spindlelike activity associated with coma is even more continuous than shown here, and unreactive. The term "spindle coma" is reserved for patients known to be comatose.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Triphasic waves. Note the near continuous pattern of periodic triphasic waveforms, with a large frontal positivity (downgoing) preceded and followed by smaller negative deflections. The wave marked near the middle of the sample illustrates the classic anterior-posterior lag. This pattern is typically unreactive. Note that a triphasic morphology is necessary but not sufficient to classify a pattern as "triphasic waves."



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Benbadis SR, Tatum WO: Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000 Nov 14; 55(9): 14213[Medline]. Geller E: Generalized disturbances of brain function: encephalopathies, coma, degenerative diseases, and brain death. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:438-455. Kaplan PW, Genoud D, Ho TW, Jallon P: Etiology, neurologic correlations, and prognosis in alpha coma. Clin Neurophysiol 1999 Feb; 110(2): 205-13[Medline]. Kaplan PW, Genoud D, Ho TW, Jallon P: Clinical correlates and prognosis in early spindle coma. Clin Neurophysiol 2000 Apr; 111(4): 584-90[Medline]. Levin KH, Lüders HO, eds: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000. Lüders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000.

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eMedicine - EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns : Article by Selim R Benbadis, MD Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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eMedicine - EEG Atlas: Epileptiform Normal Variants : Article by Selim R Benbadis, MD


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Synonyms and related keywords: benign epileptiform transients of sleep, midline theta, phantom spikes and waves, psychomotor variants, small sharp spikes, subclinical rhythmic EEG discharges of adults, wicket spikes, 14- and 6-Hz positive spikes AUTHOR INFORMATION



Section 1 of 6


Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Paul E Barkhaus, MD, Director, Division of Neuromuscular Diseases, Milwaukee Veterans Administration Medical Center; Professor, Department of Neurology, Medical College of Wisconsin; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

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Epileptiform normal variants are EEG patterns that resemble epileptogenic abnormalities. Most of these patterns initially were thought to be associated with epilepsy or other neurological conditions but subsequently were demonstrated to have no such significance. They now are considered normal variants of no clinical significance. Their recognition is important to avoid overinterpretation or misinterpretation with regard to their significance. This article reviews the following such patterns: small sharp spikes (SSS), wicket spikes, 14- and 6-Hz positive spikes, phantom spike and waves, psychomotor variants, subclinical rhythmic EEG discharges of adults (SREDA), and midline theta. Most of these patterns initially were described in the 1950s. Gibbs and Gibbs described small sharp spikes in 1952, and 14- and 6-Hz positive spikes were described at approximately the same time (Gibbs and Gibbs, 1951;






Grossman, 1954; Kellaway et al, 1959; Nidermeyer and Croft, 1961). The 6-Hz phantom spike-wave was described by Walter (1950), and the psychomotor variant was described by Gibbs and Gibbs (1952). Wickets were described in 1977 (Reiher and Lebel). WAVEFORM DESCRIPTIONS

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Small sharp spikes (Images 1-3): Also known as benign epileptiform transients of sleep (BETS), SSSs occur in light sleep (stages I and II of nonrapid eye movement [NREM] sleep), usually sporadically. Location is temporal, either unilateral or bilaterally independent, and with a broad field of distribution. Morphology is typically monophasic, occasionally diphasic, and the decline after the first negative peak is very steep. SSSs rarely may have a single aftergoing slow-wave component but generally are not disturbing the background. The main features of SSSs are in their name: duration is short, amplitude is small, and an easy guideline states that SSSs generally should be less than 50 mV and less than 50 milliseconds. Wicket spikes (Images 4-6): Wicket spikes occur in both awake state and light sleep. Frequency is 6-11 Hz, usually in short runs (“wicket rhythm”) but also as single sharp transients. Location is temporal, usually bilateral and independent. Morphology is archlike or mu-like, sharp, monophasic, and not followed by an aftergoing slow wave. Amplitude may be high, but the transient arises out of an ongoing rhythm and does not "stand out." 14-Hz and 6-Hz positive spikes: This pattern is observed at any age, but it is expressed maximally in adolescents, especially those aged 13-14 years (Klass and Westmoreland, 1985). The 6-Hz positive spikes predominate in children younger than 1 year and in adults older than 40 years, and the 14-Hz positive spikes predominate or combine with 6-Hz spikes in the other age groups (Gibbs et al, 1963). Both 14- and 6-Hz positive spikes are observed predominantly during light sleep. These spikes usually appear in short runs lasting less than 2 seconds, and their frequencies, as the name implies, are 14 Hz and 6 Hz. Location is mostly posterior temporal, unilaterally or bilaterally. Morphology is a sharply contoured positive spike alternating with rounded negative component. Amplitude is medium, around 20-60 µV. Phantom spike and wave (6 Hz): The 6-Hz spike and wave pattern may be observed in both adolescents and adults. It generally occurs during relaxed wakefulness and stage I sleep and disappears during deeper levels of sleep. Frequency is 6 Hz, and the bursts last 1-2 seconds. Location is usually diffuse, bisynchronous, and relatively symmetric. This pattern may predominate in the anterior and posterior head regions. Morphology is a typically small (<30 µV and <30 ms), evanescent diphasic spike followed by a higher (50-100 µV) slow wave component. Thus, the spike component may be difficult to see. Psychomotor variant (Image 7): A more useful and descriptive term is rhythmic midtemporal theta of drowsiness (RMTD). Frequency is theta (4-7 Hz). Location is maximum midtemporal, unilateral or bilaterally independent or bisynchronous. Morphology typically is notched, flat topped, or sharply contoured. Bursts may last 1-10 seconds or longer and thus resemble temporal lobe seizures. Amplitude is medium to high. Subclinical rhythmic EEG discharges of adults: SREDA is an uncommon pattern observed mainly in older persons (>50 y). It may occur at rest or during drowsiness. SREDA superficially resembles an EEG seizure pattern. Frequency is typically 5-6 Hz. Location is widespread or bilateral with a posterior maximum. Morphology is seizurelike (ie, rhythmic sharply contoured theta). Abrupt onset and termination may help distinguish SREDA from an EEG seizure. Duration ranges from 20 seconds to minutes (average 40-80 s). Midline theta rhythm (ie, Ciganek rhythm): Midline theta rhythm may be observed during wakefulness or drowsiness. As indicated by the name, frequency is 4-7 Hz, and the location is midline (ie, vertex). Morphology is rhythmic, smooth, sinusoidal, arciform, spiky, or mu-like. CLINICAL CORRELATION

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As a whole, these normal variants need to be differentiated from epileptiform discharges (ie, spikes, sharp waves, spike-wave complexes; see Generalized EEG Waveform Abnormalities). In general, the benign patterns lack the characteristics of pathological epileptiform discharges, high amplitude and aftergoing slow wave or suppression, making them “disturbing” to the background activity. By default, assume that sharp transients are



benign variants, and consider them epileptiform and abnormal only if they do not meet criteria for any benign transients. SSS are generally easy to distinguish from spikes because of their short duration and small amplitude. The 14- and 6-Hz positive spikes should not be confused with temporal spikes because of their characteristic polarity (epileptiform spikes are almost always surface negative in polarity) and typical frequency. Phantom spike and waves (6 Hz) may be difficult to distinguish from the definitive clinically significant spike and wave complexes. A helpful way to distinguish them is by the tendency of benign phantom spike and waves (6 Hz) to disappear during sleep; epileptiform discharges (spike and wave complexes) tend to persist or become more prominent with deeper levels of sleep. Psychomotor variant differs from a seizure discharge because it is usually a monomorphic or monorhythmic pattern that does not evolve into other frequencies or waveforms as usually occurs during seizures. Wicket spikes commonly are misinterpreted as sharp waves, especially when they occur as single sharp transients. Examining the context and whether they arise out of an ongoing rhythm is important. Wickets predominate in adults older than 30 years and have an incidence of 0.9% (Reiher and Lebel, 1977). SREDA is never associated with symptoms, in contrast to a seizure pattern. Midline theta rhythm does not have any clinical significance and appears to represent a nonspecific variant of theta activity. As with many others, this pattern initially was believed to occur predominantly in patients with temporal lobe epilepsy. Later reviews have shown that the Ciganek rhythm represents a nonspecific variant of theta activity (Mokran et al, 1971; Westmoreland and Klass, 1986). PICTURES

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Caption: Picture 1. EEG atlas: epileptiform normal variants. A small sharp spike is present in the left temporal region (modified double banana montage). Note the widespread field of distribution (isopotential at F7, T1, and T3), low amplitude (<50 mA), and short duration (<50 ms).



Picture Type: Photo Caption: Picture 2. EEG atlas: epileptiform normal variants. Left temporal small sharp spike. Note low amplitude (<50 mA) and short duration (<50 ms).





Picture Type: Photo Caption: Picture 3. EEG atlas: epileptiform normal variants. A small sharp spike is present in the right temporal region. Note the low amplitude (<50 mA) and short duration (<50 ms).



Picture Type: Photo Caption: Picture 4. EEG atlas: epileptiform normal variants. Wicket spikes in the left temporal region. Note the sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope giving the “wicket” morphology.



Picture Type: Photo Caption: Picture 5. EEG atlas: epileptiform normal variants. Wicket spikes in the left temporal region. Note the sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope, giving the wicket morphology.



Picture Type: Photo



Caption: Picture 6. EEG atlas: epileptiform normal variants. Wicket spikes in the left temporal region. Note the sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope, giving the wicket morphology.



Picture Type: Photo Caption: Picture 7. EEG atlas: epileptiform normal variants. Rhythmic midtemporal theta of drowsiness or psychomotor variant. Note the seizurelike rhythmicity and notched morphology.



Picture Type: Photo Caption: Picture 8. PowerPoint presentation, EEG epileptiform normal variants


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Benbadis SR, Tatum WO IV: Over-intepretation of EEGs and misdiagnosis of epilepsy. In press. Ciganek L: Theta-discharges in the middle-line—EEG symptom of temporal lobe epilepsy. Electroencephalogr Clin Neurophysiol 1961; 13: 669-673. Daly DD, Pedley TA: Current Practice of Clinical Electroencephalography. 2nd ed. New York, NY: Raven Press; 1990:243-251. Engel J Jr: A practical guide for routine EEG studies in epilepsy. J Clin Neurophysiol 1984 Apr; 1(2): 109-42[Medline]. Garvin JS: Psychomotor variant pattern. Dis Nerv Syst 1968 May; 29(5): 307-9[Medline]. Gibbs EL, Gibbs FA: Atlas of Electroencephalography. Vol 2. Cambridge, Mass: Addison-Wesley; 1952:346-358. Gibbs EL, Gibbs FA: Electroencephalographic evidence of thalamic and hypothalamic epilepsy. Neurology 1951; 1: 136-144. Gibbs FA, Gibbs EL: Atlas of Electroencephalography. Vol 3. Reading, Mass: Addison–Wesley; 1964. Gibbs FA, Rich CL, Gibbs EL: Psychomotor variant type of seizure discharge. Neurology (Minneap) 1963; 13: 991-998. Gibbs FA, Gibbs EL: Fourteen and six per second positive spikes. Electroencephalogr Clinical Neurophysiol 1963; 15: 553-558. Grossman C: Laminar cortical blocking and its relation to episodic aggressive outbursts. Arch Neurol Psychiat (Chicago) 1954; 71: 576-587. Hughes JR, Schlagenhauff RE, Magoss M: Electroclinical correlations in the six per second spike and wave complex. Electroencephalogr Clin Neurophysiol 1965; 18: 71-75. Kellaway P, Crawley JW, Kagawa NA: A specific electroencephalographic correlate of convulsive equivalent disorders in children. J Pediatr 1959; 55: 582-592. Klass DW, Westmoreland BF: Nonepileptogenic epileptiform electroencephalographic activity. Ann Neurol 1985 Dec; 18(6): 62735[Medline]. Lombroso CT, Schwartz IH, Clark DM: Ctenoids in healthy youths. Controlled study of 14- and 6-per-second positive spiking. Neurology 1966 Dec; 16(12): 1152-8[Medline]. Luders HO, Noachtar S: Atlas and Classification of Electroencephalography. Philadelphia, Pa: WB Saunders Co; 2000. Marshall C: Some clinical correlates of the wave and spike phantom. Electroencephalogr Clin Neurophysiol 1955; 7: 633-636.


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Maulsby RL: EEG patterns of uncertain diagnostic significance. In: Klass DW, Daly DD, eds. Current Practice of Clinical Electroencephalography. NY: Raven Press; 1979:411-419. Miller CR, Westmoreland BF, Klass DW: Subclinical rhythmic EEG discharges of adults (SREDA): Further observations. Am J EEG Technol 1985; 25: 217-224. Mokran V, Ciganek L, Kabatnik Z: Electroencephalographic theta discharges in the midline. Eur Neurol 1971; 5(5): 288-93[Medline]. Nidermeyer E, Croft JR: Uber die bedeutung der 14 and 6 per sec positiven spitzen im EEG. Archiv fur phychiatrie und Nervenkrankeiter (Berlin) 1961; 202: 266-280. Pedley TA: EEG pattern that mimic epileptiform discharges but have no association with seizures. In: Henry CE, ed. Current Clinical Neurophysiology: Update on EEG and Evoked Potentials. NY: Elsevier Science; 1980:307-336. Reiher J, Lebel M: Wicket spikes: clinical correlates of a previously undescribed EEG pattern. Can J Neurol Sci 1977 Feb; 4(1): 3947[Medline]. Silverman D: Phantom spike-waves and the fourteen and six per second positive spike pattern: a consideration of their relationship. Electroencephalogr Clin Neurophysiol 1967 Sep; 23(3): 207-13[Medline]. Small JG: Small sharp spikes in a psychiatric population. Arch Gen Psychiatry 1970 Mar; 22(3): 277-84[Medline]. Small JG, Sharpley P, Small IF: Positive spikes, spike-wave phantoms, and psychomotor variants: A survey of these EEG patterns in psychiatric patients. Arch Gen Psychiatry 1968; 18: 232-238. Thomas JE, Klass DW: Six-per-second spike-and-wave pattern in the electroencephalogram. A reappraisal of its clinical significance. Neurology 1968 Jun; 18(6): 587-93[Medline]. Walter WG: Epilepsy. In: Hill D, Parr G, eds. Electroencephalography: A Symposium on Its Various Aspects. London: Mcdonald & Company; 1950:228-272. Westmoreland BF, Klass DW: A distinctive rhythmic EEG discharge of adults. Electroencephalogr Clin Neurophysiol 1981 Feb; 51(2): 186-91[Medline]. Westmoreland BF, Klass DW: Midline theta rhythm. Arch Neurol 1986 Feb; 43(2): 139-41[Medline]. White JC, Langston JW, Pedley TA: Benign epileptiform transients of sleep. Clarification of the small sharp spike controversy. Neurology 1977 Nov; 27(11): 1061-8[Medline]. Wiener JM, Delano JG, Klass DW: An EEG study of delinquent and nondelinquent adolescents. Arch Gen Psychiatry 1966; 15: 144150.


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eMedicine - EEG Atlas: Focal (Nonepileptic) Abnormalities : Article by Selim R Benbadis, MD


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EEG Atlas: Focal (Nonepileptic) Abnormalities

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Last Updated: March 8, 2002

Synonyms and related keywords: slowing, delta slowing, slow activity, amplitude asymmetry, periodic epileptiform lateralized discharges, PLED AUTHOR INFORMATION

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Section 1 of 6


Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida



Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Paul E Barkhaus, MD, Director, Division of Neuromuscular Diseases, Milwaukee Veterans Administration Medical Center; Professor, Department of Neurology, Medical College of Wisconsin; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

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Before the advent of modern neuroimaging, EEG was the best noninvasive tool to use in searching for focal lesions. In the last few decades, with progress in imaging techniques, the role of EEG is changing; its use for localization of a brain lesion is being superseded by neuroimaging. The utilization of EEG outside of epilepsy has declined markedly. The use of EEG in monitoring brain activity in the operating room and also in intensive care settings needs to be redefined and its utility reassessed. In clinical situations in which the primary question is the electrical functioning of the brain and not primarily localization, EEG will remain a necessary test. EEGs are performed routinely in various clinical situations; therefore the neurophysiologist is expected to be familiar with the EEG findings even in situations in which they are of relatively limited value.




Like most neurophysiologic tests, EEG is a test of cerebral function; hence for the most part it will be nonspecific as to etiology. Although at one time authors discussed the application of EEG in differentiating various types of lesions, this clearly has not been clinically useful in the modern era. The exercise of describing EEG abnormalities by pathology (eg, stroke, abscess, tumor, even various types of tumors!), which was common in old EEG texts, is therefore not followed here. Instead, the different patterns of focal (nonepileptic) disturbances of brain function and their clinical significance are reviewed. WAVEFORM DESCRIPTIONS

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Slow activity Abnormal slow activity is by far the most common EEG manifestation of focal brain dysfunction. The abnormality that correlates best with the presence of a structural lesion is polymorphic or arrhythmic (as opposed to monomorphic or rhythmic) delta (ie, 1-3 Hz) slowing. This is all the more reliable when it is continuous, unreactive (ie, characterized by lack of change between states, such as wake or sleep, or in response to external stimuli), of high amplitude, polymorphic, and unilateral. The localization of slow potentials follows the same rules as that of epileptiform discharges. Thus, “phase reversals” are useful to localize slow potentials and do not imply abnormality or epileptogenicity. Amplitude asymmetry In the classification used here, the term asymmetry refers to asymmetry of amplitude and to normal rhythms. By contrast, a focal frequency asymmetry would be classified as focal slow (Lüders and Noachtar). Finally, readers should keep in mind that amplitude asymmetries should be evaluated on referential montages, since amplitude is highly dependent on interelectrode distances. Periodic lateralized epileptiform discharges Described in 1964 by Chatrian et al, periodic lateralized epileptiform discharges (PLEDS) are a special type of focal abnormality. As implied by their name, they are periodic, lateralized, and epileptiform. Periodicity is the most characteristic feature, and the one that sets PLEDS apart from other focal abnormalities. Periodicity refers to a relatively constant interval between discharges, which varies between 0.5 and 3 seconds and most often is around 1 second. The epileptiform morphology of the discharges is not invariable, as PLEDS are often closer to slow waves than to sharp waves in morphology. CLINICAL CORRELATION

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Slow activity Continuous focal slow activity is the only nonepileptiform focal abnormality that can be interpreted unequivocally as abnormal when it is an isolated finding. Other focal abnormalities are quite frequent but are of such low specificity that they almost never constitute an abnormality in themselves. To be interpreted as abnormal, these usually require the coexistence of a more definite abnormality such as slowing or epileptiform discharges. As already outlined, focal slowing is nonspecific as to etiology, and in the era of neuroimaging the EEG has no role in diagnosing the nature of a lesion. Focal slowing is the most common abnormality associated with focal lesions of any type, including (but not limited to) neoplastic, vascular, subdural collections, traumatic, and infectious (see Images 1-4). It occasionally may be seen even in more subtle structural abnormalities such as mesiotemporal sclerosis or focal malformations of cortical development. The physiologic basis for focal polymorphic delta activity caused by focal cortical lesions is not fully understood. It is probably due to abnormalities in the underlying white matter rather than the cortex itself. When present, focal slow activity correlates highly with the side of the lesion, but it is not reliable for lobar localization. The likelihood of a structural lesion (ie, specificity) diminishes when the slow activity lacks these characteristics and is intermittent (see Image 5), in the theta rather than the delta range, and of low amplitude. This type of slowing may be normal (eg, temporal slowing of the elderly; see the article Normal EEG Variants). This is essentially the http://www.emedicine.com/neuro/topic703.htm (2 of 7) [4/9/2003 2:43:40 PM]


difference between focal “continuous slow” and “intermittent slow” (Lüders and Noachtar). In a few situations in clinical neurology, the EEG may show clear evidence of focal dysfunction (ie, focal slow) while no structural abnormality is found. The typical cases in point are the focal epilepsies. A readily demonstrable structural lesion usually is not found on neuroimaging, typically MRI (see EEG Atlas: Localizationrelated Epilepsies). Focal brain dysfunction without structural abnormalities has been observed in transient ischemic attacks (TIA), migraine, and postictal states. Polymorphic delta activity in these cases may be indistinguishable from that caused by a structural lesion, except that it is short-lived (ie, it disappears over time). The postictal state is the most common cause of nonstructural polymorphic delta activity, but the activity disappears within minutes to hours after the ictal event. Patients with ongoing TIAs or migraine rarely undergo an EEG during the symptomatic period, so clinical data are scarce. Amplitude asymmetry Destructive lesions clearly can attenuate the amplitude of normal rhythms. However, normal rhythms are never perfectly symmetric in amplitude, therefore which asymmetries to consider significant is not always clear. (Some have proposed a greater than 50% side-to-side difference as abnormal.) A good rule of thumb is that, with very few exceptions, significant focal asymmetries are associated with slowing. The authors recommend that any amplitude asymmetry associated with slowing of frequency be considered significant. Amplitude asymmetry or suppression of normal rhythms is somewhat more likely to be seen in structural abnormalities that increase the distance or interfere with the conduction of the electrical signal between the cortex and the recording scalp electrodes. Examples include subdural collections (eg, hematoma, empyema), epidural collections (eg, hematoma, abscess), subgaleal collections, and calcifications such as those seen in Sturge-Weber syndrome. Amplitude asymmetry also may be more common than slowing in subdural hematomas. However, caution must be exercised before considering isolated nonepileptiform focal findings other than slowing as abnormal. In general, as with other types of focal EEG abnormalities such as slowing, amplitude asymmetry is nonspecific as to etiology. Although asymmetry in amplitude is usually indicative of dysfunction on the side of depressed amplitude, one notable exception to this rule is the so-called breach rhythm (see Image 6). This is caused by a skull defect, which attenuates the high-frequency filter function of the intact skull. As a result, faster frequencies (eg, alpha, spindles, beta) are of higher amplitude on the side of the defect. Since morphology often is sharply contoured, determining the epileptogenicity of these discharges can be extremely difficult, and in this situation erring on the conservative side, by not interpreting them as epileptiform, is clearly preferable. Because of a cancellation effect between frontopolar (Fp1/Fp2) and frontal (F3/F4), eye movements often are not increased on the side of a skull defect and may indeed be of lesser amplitude on that side. Periodic lateralized epileptiform discharges PLEDS are caused by acute destructive focal lesions and are a transitory phenomenon: they tend to disappear in weeks, even if the causal lesion persists. Over time, the record takes on a less specific focal slow appearance, which is more likely to persist. By far the most common etiology is an acute cerebrovascular event; second most common is focal encephalitis such as that caused by herpes. In a clinical context suggestive of viral encephalitis, the EEG can be of great value for diagnosis and can guide tissue biopsy. Though most often associated with an acute destructive lesion, PLEDS, like other EEG findings, are not specific as to etiology and have been described in almost all types of structural lesions, including subdural hematoma and chronic lesions, especially in the presence of a superimposed systemic disturbance. In keeping with their epileptiform morphology, PLEDS have a close association with clinical seizures, and on average about 80% of patients with PLEDS have clinical seizures (see Images 7-8). The transition between PLEDS and a clear ictal seizure pattern is very gradual, illustrating the hypothesis that PLEDS may represent a subclinical ictal pattern. In clinical practice, however, PLEDS usually are managed as interictal discharges (ie, spikes or sharp waves). They indicate a high risk for focal seizures, but usually are not treated with antiepileptic drugs unless clinical evidence for seizures is noted. This position is endorsed by the authors and others. This is



somewhat controversial, however, and some advocate antiepileptic treatment in all patients with PLEDS. Periodic patterns in Creutzfeldt-Jakob disease usually are generalized and bisynchronous (see articles on encephalopathies) but occasionally, especially early in the course, they may be unilateral or markedly asymmetric, and thus take on the appearance of PLEDS. Other less common focal patterns An abnormal response to photic stimulation can be seen in focal lesions. Normal photic driving has long been known to be potentially reduced on the side of a lesion. Posterior destructive lesions are particularly likely to attenuate the driving response, but some reports have described an enhanced photic response on the side of dysfunction. However, since the normal driving response can be quite asymmetric, such a finding should be accompanied by a more reliable abnormality such as slowing of the waveform frequency in order to be interpreted as abnormal. The Bancaud phenomenon refers to the unilateral loss of reactivity of a normal rhythm and initially was described in the context of the alpha rhythm. It should be considered a pathological finding only when associated with other more definite abnormalities, such as slowing. PICTURES

Section 5 of 6


Caption: Picture 1. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, lateralized right hemisphere. While “spilling over” to the left frontal region, the polymorphic delta activity is clearly predominant over the right hemisphere. This type of slowing almost invariably is associated with a structural hemispheric lesion. This patient had a large right middle cerebral artery infarct.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, lateralized left hemisphere. This polymorphic delta activity was continuous throughout the record. This patient had a left hemisphere neoplasm.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, regional right temporal. This polymorphic delta activity is somewhat more focal than that shown in Image 1, with a maximum in the temporal chain. Little such activity is evident in the central chain, but enough to exclude a T4 electrode artifact. The slowing shows phase reversals at T4, indicating a maximum at that electrode.





Picture Type: Photo Caption: Picture 4. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, regional left temporal. This polymorphic delta activity is somewhat more focal than that in Image 2, with a maximum in the temporal chain. The phase reversals at T3 indicate a maximum at that electrode.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 5. EEG atlas: focal (nonepileptiform) abnormalities. Intermittent slow, lateralized left hemisphere. This brief burst of delta activity is seen in the temporal and central areas. This is a much “weaker” finding than continuous slowing, and much less reliably associated with a structural lesion. This is indicative of mild dysfunction in that region.



Picture Type: Photo Caption: Picture 6. EEG atlas: focal (nonepileptiform) abnormalities. Asymmetry, increased beta, regional right frontocentral. The beta activity is increased in amplitude in the right frontocentral region. This is a “breach rhythm” and is caused most often by a skull defect (in this case a burr hole).


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 7. EEG atlas: focal (nonepileptiform) abnormalities. Periodic lateralized epileptiform discharges (PLEDS), regional left centrotemporal. The repetitive discharges occur with a periodicity of about 1 second. Polymorphic delta activity is seen over the left hemisphere, but the classification as PLEDS already implies severe focal dysfunction. In addition, it indicates an acute destructive process and very high (80%) risk of seizures.





Picture Type: Photo Caption: Picture 8. EEG atlas: focal (nonepileptiform) abnormalities. Periodic lateralized epileptiform discharges (PLEDS), lateralized right hemisphere. The repetitive discharges occur with a periodicity of 2-4 seconds. PLEDS are associated with severe focal dysfunction and with acute destructive processes and very high (80%) risk of seizures.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 9. EEG atlas: focal (nonepileptiform) abnormalities. PowerPoint presentation of Images 1-8.


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Au WJ, Gabor AJ, Vijayan N, Markand ON: Periodic lateralized epileptiform complexes (PLEDs) in Creutzfeldt- Jakob disease. Neurology 1980 Jun; 30(6): 611-7[Medline]. Bancaud J, Hécaen H, Lairy GC: Modifications de la réactivité EEG, troubles des fonctions symboliques et troubles confusionnels dans les lésions hémisphériques localisées. Electroencephalogr Clin Neurophysiol 1955; 7: 179. Benbadis S: Focal disturbances of brain function. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:457-467. Brenner RP, Schaul N: Periodic EEG patterns: classification, clinical correlation, and pathophysiology. J Clin Neurophysiol 1990 Apr; 7(2): 249-67[Medline]. Brenner RP, Sharbrough FW: Electroencephalographic evaluation in Sturge-Weber syndrome. Neurology 1976 Jul; 26(7): 62932[Medline]. Cantor FK, Ilbag F: Facilitation of photic response by focal lesions. Electroencephalogr Clin Neurophysiol 1973 Jan; 34(1): 779[Medline]. Chatrian GE, Shaw CM, Leffman F: The significance of periodic lateralized epileptiform discharges in EEG: an electrographic, clinical, and pathological study. Electroencephalogr Clin Neurophysiol 1964; 17: 177-193. Chu NS: Periodic lateralized epileptiform discharges with preexisting focal brain lesions. Role of alcohol withdrawal and anoxic encephalopathy. Arch Neurol 1980 Sep; 37(9): 551-4[Medline]. Cobb WA, Guiloff RJ, Cast J: Breach rhythm: the EEG related to skull defects. Electroencephalogr Clin Neurophysiol 1979 Sep; 47(3): 251-71[Medline]. Collice M, Arena O, Fontana RA, et al: Role of EEG monitoring and cross-clamping duration in carotid endarterectomy. J Neurosurg 1986 Dec; 65(6): 815-9[Medline]. Erkulvrawatr S: Occurrence, evolution and prognosis of periodic lateralized epileptiform discharges in EEG. Clin Electroencephalogr 1977; 8: 89-99. Faught E: Current role of electroencephalography in cerebral ischemia. Stroke 1993 Apr; 24(4): 609-13[Medline]. Fischer-Williams M, Last SL, Lyberi G, Northfield DW: Clinico-EEG study in 128 gliomas and 50 intracranial tumours. Brain 1962; 78: 42-58. Furlan AJ, Henry CE, Sweeney PJ, Mitsumoto H: Focal EEG abnormalities in Heidenhain's variant of Jakob-Creutzfeldt disease. Arch Neurol 1981 May; 38(5): 312-4[Medline]. Gambardella A, Gotman J, Cendes F, Andermann F: Focal intermittent delta activity in patients with mesiotemporal atrophy: a reliable marker of the epileptogenic focus. Epilepsia 1995 Feb; 36(2): 122-9[Medline].


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Geller E: Generalized disturbances of brain function: encephalopathies, coma, degenerative diseases, and brain death. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:438-455. Gilmore PC, Brenner RP: Correlation of EEG, computerized tomography, and clinical findings. Study of 100 patients with focal delta activity. Arch Neurol 1981 Jun; 38(6): 371-2[Medline]. Gloor P, Ball G, Schaul N: Brain lesions that produce delta waves in the EEG. Neurology 1977 Apr; 27(4): 326-33[Medline]. Heye N, Cervos-Navarro J: Focal involvement and lateralization in Creutzfeldt-Jakob disease: correlation of clinical, electroencephalographic and neuropathological findings. Eur Neurol 1992; 32(5): 289-92[Medline]. Joynt RJ, Cape CA, Knott JR: Significance of focal delta activity in adult electroencephalography. Arch Neurol 1965; 12: 631-638. Levin KH, Lüders HO, eds: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000. Lüders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000. Maytal J, Novak GP, Knobler SB, Schaul N: Neuroradiological manifestations of focal polymorphic delta activity in children. Arch Neurol 1993 Feb; 50(2): 181-4[Medline]. Michel B, Gastaut JL, Bianchi L: Electroencephalographic cranial computerized tomographic correlations in brain abscess. Electroencephalogr Clin Neurophysiol 1979 Mar; 46(3): 256-73[Medline]. Musil F: Development of focal changes in the EEG of those with cranio-cerebral injury. Electroencephalogr Clin Neurophysiol 1969 Feb; 26(2): 229[Medline]. Neufeld MY, Vishnevskaya S, Treves TA, et al: Periodic lateralized epileptiform discharges (PLEDs) following stroke are associated with metabolic abnormalities. Electroencephalogr Clin Neurophysiol 1997 Apr; 102(4): 295-8[Medline]. Pfurtscheller G, Sager W, Wege W: Correlations between CT scan and sensorimotor EEG rhythms in patients with cerebrovascular disorders. Electroencephalogr Clin Neurophysiol 1981 Nov; 52(5): 473-85[Medline]. Pohlmann-Eden B, Hoch DB, Cochius JI, Chiappa KH: Periodic lateralized epileptiform discharges--a critical review. J Clin Neurophysiol 1996 Nov; 13(6): 519-30[Medline]. Raymond AA, Fish DR: EEG features of focal malformations of cortical development. J Clin Neurophysiol 1996 Nov; 13(6): 495506[Medline]. Schaul N, Green L, Peyster R, Gotman J: Structural determinants of electroencephalographic findings in acute hemispheric lesions. Ann Neurol 1986 Dec; 20(6): 703-11[Medline]. Schwartz MS, Prior PF, Scott DF: The occurrence and evolution in the EEG of a lateralized periodic phenomenon. Brain 1973 Sep; 96(3): 613-22[Medline]. Snodgrass SM, Tsuburaya K, Ajmone-Marsan C: Clinical significance of periodic lateralized epileptiform discharges: relationship with status epilepticus. J Clin Neurophysiol 1989 Apr; 6(2): 159-72[Medline]. Upton A, Gumpert J: Electroencephalography in the early diagnosis of herpes simplex encephalitis. Rev Electroencephalogr Neurophysiol Clin 1971 Jan-Mar; 1(1): 81-3[Medline]. Vignadndra V, Ghee LT, Chawla J: EEG in brain abscess: its value in localization compared to other diagnostic tests. Electroencephalogr Clin Neurophysiol 1975 Jun; 38(6): 611-22[Medline].


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eMedicine - EEG Atlas: Generalized Epilepsies : Article by Selim R Benbadis, MD


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The International Classification of Epileptic Syndromes and Epilepsies (International League Against Epilepsy [ILAE],1989) classifies the epilepsies along 2 dichotomies: partial (ie, localization-related) vs generalized, and idiopathic vs cryptogenic or symptomatic. This double dichotomy conveniently allows the epilepsy classification system to be presented in a simple 2 x 2 table (Table 1). Table 1. Classification of the Epilepsies*

Generalized

Localization-related


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Idiopathic (genetic)

Childhood absence epilepsy Juvenile absence epilepsy Juvenile myoclonic epilepsy Epilepsy with grand-mal seizures on awakening Other idiopathic generalized epilepsies

Benign focal epilepsy of childhood (2 types) ADNFLE** Primary reading epilepsy

Symptomatic or cryptogenic

West syndrome Lennox-Gastaut syndrome Other symptomatic generalized epilepsies

Mesiotemporal lobe epilepsy Neocortical focal epilepsy

* Adapted from Tich and Pereon (1999) ** ADNFLE - Autosomal dominant nocturnal frontal lobe epilepsy The term “idiopathic” often is misunderstood in this setting and requires clarification. Whereas the term idiopathic in medicine usually means “of unknown cause,” idiopathic epilepsies are not truly of “unknown cause” (this confusing terminology will most likely be corrected in the upcoming International League Against Epilepsy (ILAE) classification system [Engel 1998]). In epilepsy, idiopathic seizures are genetically determined and have no apparent structural cause, with seizures as the only manifestation of the condition. Findings of the neurologic examination and neuroimaging studies are normal, and EEG findings also are normal other than the epileptiform abnormalities. In some syndromes the genetic substrate has even been identified. Most idiopathic epilepsies are generalized, but a few genetic epilepsies are focal. Nonidiopathic epilepsies are by definition not genetic (although some may be associated with a minor genetic predisposition), but are the result of a brain insult or lesion. If the damage is focal, it results in a localization-related epilepsy; if it is diffuse, it results in a generalized epilepsy. The difference between symptomatic and cryptogenic is subtle: symptomatic means that the etiology is known, while cryptogenic means that an underlying etiology is apparent but cannot be documented objectively. Thus the boundary between the 2 is largely dependent on our diagnostic and imaging techniques. This review discusses EEG findings in the generalized epilepsies. WAVEFORM DESCRIPTIONS

Section 3 of 6


Spikes and sharp waves are sharp transients that have a strong association with epilepsy. The two are distinguished by their duration (spikes <70 ms, sharp waves 70-200 ms), but no difference is noted in terms of clinical significance. Several characteristics distinguish these from benign epileptiform variants (see article EEG Atlas: Focal (Nonepileptic) Abnormalities), including high amplitude that makes them “stand out” from ongoing background activity and aftergoing slow waves, which give the appearance of their “disrupting” background activity (see Images 1-2). Spike-wave complexes (SWC) are the repetitive occurrence of a spike followed by a slow wave. Since any significant spike or sharp wave usually is followed by a slow wave (see above), a run of 3 seconds is required to classify a record as SWC, as opposed to the categories already mentioned (spike or sharp wave). SWC can be divided further into 2 more specific types, as follows: ●

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3-Hz SWC: This pattern is characterized by a frequency of 2.5-4 Hz and a very monomorphic (“perfectly regular”) morphology (see Image 3). It occurs in very discrete bursts, and between bursts the EEG is normal. Slow SWC: This pattern is not only slower (<2.5 Hz) but also more irregular (less monomorphic) than the 3-Hz SWC. Bursts are less discrete than the 3-Hz SWC, and between bursts other abnormalities are seen in symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type (see Images 4-5).

Polyspikes are multiple repetitive spikes occurring at about 20 Hz (see Image 6).



Generalized epileptiform discharges (ie, spikes, sharp waves, SWCs) are usually maximal in the frontal regions, with typical phase reversals at the F3 and F4 electrodes (see Image 7). Hypsarrhythmia is defined as continuous (during wakefulness), high-amplitude (>200 Hz), generalized polymorphic slowing with no organized background and multifocal spikes (see Images 8-9). Electrographic seizures ●

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Electrodecrement consists of abrupt attenuation (“flattening”) of background activity, often preceded by a high-amplitude transient (see Image 10). This typically is associated with infantile spasms or atonic seizures. Generalized paroxysmal fast activity (GPFA) consists of bursts of fast (10 Hz) activity and typically is associated with tonic seizures.


Section 4 of 6


Idiopathic generalized epilepsies These syndromes, formerly called primary generalized epilepsies, are the best known group of idiopathic epilepsies. They epitomize the meaning of the term idiopathic: genetic basis, normal neurologic examination findings, and normal intelligence. EEG shows generalized epileptiform discharges and may show photosensitivity. Seizure types include generalized tonic-clonic (GTC), absence, and myoclonic. Accordingly, EEG typically shows generalized spikes or sharp waves, 3-Hz or faster SWCs (clinically associated with absence seizures), and polyspikes (clinically associated with myoclonic seizures). The EEG is normal (ie, no abnormal slowing) except for the epileptiform abnormalities. Within the group of idiopathic generalized epilepsies, distinct entities are distinguished, primarily on the basis of predominant seizure type(s) and age of onset. Some syndromes are very well individualized, while others have less clear boundaries. The major and well-defined types of idiopathic generalized epilepsies include childhood absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with grand mal seizures (sometimes referred to as grand mal on awakening). Symptomatic generalized epilepsies These are associated with diffuse brain dysfunction. The cause may be known ("symptomatic"), such as anoxic birth injury or a metabolic or chromosomal defect, or it may be unknown ("cryptogenic"). Accordingly, clinical evidence of diffuse brain dysfunction is usually present, either intellectual (ie, developmental delay or mental retardation) or motor (ie, developmental delay or cerebral palsy). Similarly, the EEG shows evidence of diffuse brain dysfunction in addition to the epileptiform abnormalities, in the form of slowing. The clinical and EEG manifestations are not specific as to etiology, but vary tremendously with age, and thus are said to be age dependent. West syndrome is the phenotype of symptomatic or cryptogenic generalized epilepsy in the first year of life and is characterized by infantile spasms, hypsarrhythmia, and developmental delay. It is an age-specific response of the immature brain to a nonspecific focal or generalized insult. Age of onset peaks between 3 and 7 months of age. Lennox-Gastaut syndrome (LGS) has an early childhood onset (age 1-8 years) and consists of multiple seizure types, mental retardation, and typical EEG findings dominated by generalized slow SWC. Seizure types include atypical absences, tonic, atonic, myoclonic, and GTC seizures. The atonic, myoclonic, tonic, and GTC seizures of LGS frequently result in unprotected falls (referred to as “drop attacks”) with injury. Besides the classic EEG pattern of generalized slow SWC, other frequent but less specific EEG findings include background slowing, generalized slowing, and multifocal spikes. During sleep, the EEG may show polyspikes and slow waves. Another typical feature of LGS is generalized paroxysmal fast activity (>10 Hz) during sleep. Many patients with symptomatic generalized epilepsy do not meet all the criteria for LGS.



PICTURES

Section 5 of 6


Caption: Picture 1. EEG atlas: generalized epilepsies. Spike, generalized. Note the high amplitude and the aftergoing background suppression and slow wave.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: generalized epilepsies. Spike, generalized. Significant spikes usually are followed by a slow wave, as shown here. This example also illustrates that generalized spikes are typically maximal frontally. This is typical of the primary (ie, idiopathic, genetic) epilepsies. If the burst lasted 3 seconds or more, it could be classified as spike-wave complexes.



Picture Type: Photo Caption: Picture 3. EEG atlas: generalized epilepsies. Sharp waves, multifocal. Sharp waves are seen at T4, T6, T5, and F3 on this 9-second segment. With other findings, this often is seen in the symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: generalized epilepsies. Slow spike-wave complexes. In addition to being slower, this is also less monomorphic than the 3-Hz spike-wave complexes. With other findings, this often is seen in the symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type.





Picture Type: Photo Caption: Picture 5. EEG atlas: generalized epilepsies. Slow spike-wave complexes (SWC). In addition to being slower, this is also less monomorphic than the 3-Hz SWC. With other findings, this often is seen in the symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: generalized epilepsies. Polyspike, generalized. Note the aftergoing slow wave. This is associated with the “primary” or idiopathic (genetic) generalized epilepsies, most typically juvenile myoclonic epilepsy.



Picture Type: Photo Caption: Picture 7. EEG atlas: generalized epilepsies. 3-Hz spike-wave complexes (SWC), generalized. This pattern is very monomorphic, with a maximum (shown here by a phase reversal) frontally, typically at F3/F4. This is typical of idiopathic (ie, genetic) generalized epilepsies, such as absence epilepsy. The 3-Hz SWC is often faster at onset (4-5 Hz), as shown here.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 8. EEG atlas: generalized epilepsies. Hypsarrhythmia. High-amplitude slowing with no organized background, and multifocal spikes (left and right frontal in this sample). This is a phenotype of the first year of life and is associated with West syndrome (ie, infantile spasms).





Picture Type: Photo Caption: Picture 9. EEG atlas: generalized epilepsies. Hypsarrhythmia. High-amplitude slowing (note the scale) with no organized background, and multifocal spikes (right frontal and left occipital in this sample). This is a phenotype of the first year of life and is associated with West syndrome (ie, infantile spasms).


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 10. EEG atlas: generalized epilepsies. Generalized paroxysmal fast activity and electrodecrement. This pattern is characteristic of the symptomatic/cryptogenic epilepsies of the LennoxGastaut type and may be subclinical or associated with tonic or atonic seizures.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 11. PowerPoint presentation of Images 1-11.


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Appleton RE, Beirne M: Absence epilepsy in children: the role of EEG in monitoring response to treatment. Seizure 1996 Jun; 5(2): 147-8[Medline]. Beaumanoir A, Bureau M, Deonna T, et al: Continuous spikes and waves during slow sleep. Electrical status epilepticus during slow sleep. Acquired epileptic aphasia and related conditions. London: John Libbey; 1995. Benbadis SR, Luders HO: Epileptic syndromes: an underutilized concept. Epilepsia 1996 Nov; 37(11): 1029-34[Medline]. Benbadis SR, Luders HO: Generalized epilepsies. Neurology 1996 Apr; 46(4): 1194-5[Medline]. Benbadis SR, Wyllie E: Pediatric epilepsy syndromes. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:468-480. Berkovic SF, Andermann F, Andermann E, et al: Concepts of absence epilepsies: discrete syndromes or biological continuum? Neurology 1987 Jun; 37(6): 993-1000[Medline]. Brenner RP, Atkinson R: Generalized paroxysmal fast activity: electroencephalographic and clinical features. Ann Neurol 1982 Apr; 11(4): 386-90[Medline]. Engel J Jr: Classifications of the International League Against Epilepsy: time for reappraisal. Epilepsia 1998 Sep; 39(9): 10147[Medline].


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Grunewald RA, Panayiotopoulos CP: Juvenile myoclonic epilepsy. A review. Arch Neurol 1993 Jun; 50(6): 594-8[Medline]. Holmes GL, McKeever M, Adamson M: Absence seizures in children: clinical and electroencephalographic features. Ann Neurol 1987 Mar; 21(3): 268-73[Medline]. Hrachovy RA, Frost JD Jr, Kellaway P: Hypsarrhythmia: variations on the theme. Epilepsia 1984 Jun; 25(3): 317-25[Medline]. International League Against Epilepsy, Commission on Classification and Terminol: Proposal for revised classification of epilepsies and epileptic syndromes . Epilepsia 1989 Jul-Aug; 30(4): 389-99[Medline]. Lancman ME, Asconapé JJ, Brotherton T, et al: Juvenile myoclonic epilepsy: an underdiagnosed syndrome. J Epilepsy 1995; 8: 215218. Lancman ME, Asconape JJ, Penry JK: Clinical and EEG asymmetries in juvenile myoclonic epilepsy. Epilepsia 1994 Mar-Apr; 35(2): 302-6[Medline]. Loiseau P, Duche B, Pedespan JM: Absence epilepsies. Epilepsia 1995 Dec; 36(12): 1182-6[Medline]. Lombroso CT: A prospective study of infantile spasms: clinical and therapeutic correlations. Epilepsia 1983 Apr; 24(2): 13558[Medline]. Lüders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000. Markand ON: Slow spike-wave activity in EEG and associated clinical features: often called 'Lennox' or "Lennox-Gastaut' syndrome. Neurology 1977 Aug; 27(8): 746-57[Medline]. Reutens DC, Berkovic SF: Idiopathic generalized epilepsy of adolescence: are the syndromes clinically distinct? Neurology 1995 Aug; 45(8): 1469-76[Medline]. Thomas P, Beaumanoir A, Genton P, et al: 'De novo' absence status of late onset: report of 11 cases. Neurology 1992 Jan; 42(1): 104-10[Medline]. Tich SN, Pereon Y: Semiological seizure classification. Epilepsia 1999 Apr; 40(4): 531[Medline]. Wyllie E, Lüders H: Classification of seizures. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 2nd ed. Baltimore: Lippincott Williams & Wilkins; 1997:355-357.


EEG Atlas: Generalized Epilepsies excerpt



eMedicine - EEG Atlas: Localization-related Epilepsies : Article by Selim R Benbadis, MD


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EEG Atlas: Localization-related Epilepsies

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Section 2 of 6


The International Classification of Epileptic Syndromes and Epilepsies (International League Against Epilepsy {ILAE], 1989) classifies the epilepsies along 2 dichotomies: partial (ie, localization-related) vs generalized, and idiopathic vs cryptogenic or symptomatic. This double dichotomy conveniently allows presentation of the epilepsy classification in a simple 2 x 2 table (Table 1). Table 1. Classification of the Epilepsies*

Generalized

Localization-related


Link to this site






Idiopathic (genetic)

Childhood absence epilepsy Juvenile absence epilepsy Juvenile myoclonic epilepsy Epilepsy with grand mal seizures on awakening Other idiopathic generalized epilepsies

Benign focal epilepsy of childhood (2 types) ADNFLE** Primary reading epilepsy

Symptomatic or cryptogenic

West syndrome Lennox-Gastaut syndrome Other symptomatic generalized epilepsies

Mesiotemporal lobe epilepsy Neocortical focal epilepsy

* Adapted from Nguyen et al (1999) ** ADNFLE - Autosomal dominant nocturnal frontal lobe epilepsy The term “idiopathic” often is misunderstood in this setting and requires clarification. Whereas the term idiopathic usually means “of unknown cause,” idiopathic epilepsies are not truly of “unknown cause” (this confusing terminology will most likely be corrected in the upcoming ILAE classification system [Engel, 1998]). Idiopathic epilepsies are determined genetically and have no apparent structural cause, with seizures as the only manifestation of the condition. Findings of the neurologic examination and imaging studies are normal, and EEG is normal other than the epileptiform abnormalities. In some syndromes the genetic substrate has even been identified. Most idiopathic epilepsies are generalized, but a few are focal. Nonidiopathic epilepsies are by definition not genetic, although some may be associated with a minor genetic predisposition; they are the result of a brain insult or lesion. If the damage is focal, it results in a localization-related epilepsy; if it is diffuse, it results in a generalized epilepsy. The difference between symptomatic and cryptogenic is subtle: symptomatic means that the etiology is known, while cryptogenic means that an underlying etiology is apparent but cannot be documented objectively. Thus the boundary between the two is largely dependent on the capabilities of our diagnostic and imaging techniques. This review discusses EEG findings in the localization-related (also known as focal or partial) epilepsies. WAVEFORM DESCRIPTIONS

Section 3 of 6


Spikes and sharp waves are sharp transients that have a strong association with epilepsy. The two are distinguished only by their duration (spikes <70 ms, sharp waves 70-200 ms), but they have no differences in terms of clinical significance. Several characteristics distinguish these from benign epileptiform variants (see article EEG Atlas: Focal (Nonepileptic) Abnormalities), including high amplitudes, which make them “stand out” from ongoing background activity, and aftergoing slow waves, which give the appearance of their “disrupting” background activity (see Images 1-6). Polyspikes are rarely focal, although focal spikes can at times have a multiphasic “polyspike-like” morphology. Electrographic seizures: Focal seizures are discharges characterized by rhythmicity and evolution (“build-up”) in frequency and amplitude. The discharge can consist of rhythmic theta or delta activity, or repetitive spikes or sharp waves, but the most characteristic features of electrographic focal seizures are rhythmicity and evolution (see Image 7).


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Idiopathic localization-related epilepsies Benign focal epilepsy of childhood is the main localization-related epilepsy that is idiopathic. Two varieties have http://www.emedicine.com/neuro/topic705.htm (2 of 6) [4/9/2003 2:46:54 PM]


been well described and are in the 1989 ILAE classification: centrotemporal and occipital. A third type has been described more recently: autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). Benign childhood epilepsy with centrotemporal spikes (BECTS) is by far the more common. Age of onset is between 4 and 12 years (peak age 8-9 years). Seizures are simple partial with motor symptoms involving the face, and they tend to occur during sleep or on awakening. Though these focal seizures are the most characteristic seizure types in BECTS, they can be quite subtle and are missed easily, so that the most common mode of presentation is a (secondary) generalized tonic-clonic seizure. As with all idiopathic epilepsy syndromes, neurologic examination findings are normal. EEG findings are characteristic, with stereotyped centrotemporal sharp waves that have a characteristic morphology. They are activated markedly by non–rapid eye movement (NREM) sleep, often occur in repetitive bursts, and can be bilateral and independent. Notably, the interictal sharp waves of BECTS often occur in asymptomatic children. In fact, only a minority of children with these discharges may have seizures. Childhood epilepsy with occipital paroxysms is less common and less consistently benign. It shares all the characteristics of an idiopathic syndrome (ie, normal findings on examination, intelligence quotient [IQ] testing, and neuroimaging studies). Age of onset is 4-8 years. Seizures are rare and primarily nocturnal, and often involve visual symptoms. Sharp waves have a maximum occipital negativity, often occur in long bursts of spikewave complexes, and are activated markedly by eye closure. ADNFLE is a recently described genetic localization-related epilepsy. Several mutations of the neuronal nicotinic acetylcholine receptor alpha4 subunit have been identified in association with this epilepsy. It has the expected features of idiopathic (ie, genetic) epilepsies, including onset early in life and normal imaging findings. Seizures are nocturnal and occur in clusters, mimicking parasomnias. They are mostly brief tonic seizures and rare (secondarily) generalized tonic-clonic convulsions, often preceded by a nonspecific aura. Interictal EEG may show epileptiform discharges with a frontal predominance, often seen only in sleep. Ictal EEG does not always show definite ictal discharges. Thus the electroclinical features of ADNFLE are not different from those of symptomatic or cryptogenic frontal lobe epilepsy. Since the genetic findings are variable (ie, locus heterogeneity), its definite diagnosis is largely one of exclusion. Cryptogenic focal epilepsies This is by far the most common type of adult-onset epilepsy. By definition, seizures arise from a localized region of the brain. If the cause is found, they are said to be symptomatic. If imaging study findings are normal, the cause remains presumptive and they are said to be cryptogenic. As stated already, the boundary between the two is largely dependent on our diagnostic and imaging techniques, and etiologies such as low-grade tumors, hippocampal sclerosis, and subtle cortical dysplasias are identified more and more often owing to advances in neuroimaging. Clinically, seizures may be simple partial or complex partial, with or without secondary generalization. Interictal EEG shows focal spikes or sharp waves, and ictal EEG shows a focal or regional discharge at onset. The main clinical entities are mesiotemporal lobe epilepsy, neocortical focal epilepsies, and hemispheric syndromes. PICTURES

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Caption: Picture 1. EEG atlas: localization-related epilepsies. Sharp waves, left temporo-occipital region. The sharp waves are, like any significant epileptiform discharges, followed by slowing and “disruption” of the background. The referential montage (right panel) confirms that the maximum is at T6, closely followed by O2.





Caption: Picture 2. EEG atlas: localization-related epilepsies. Sharp waves, left temporal region. The maximum (phase reversal) is at T3. The small sharp wave in the 4th second may not be sufficient in itself owing to its small amplitude but, in the context of the definite one, is certainly significant.



Picture Type: Photo Caption: Picture 3. EEG atlas: localization-related epilepsies. Sharp waves, left temporal region. The maximum (phase reversal) is consistently at T3. Note the associated slow activity and background attenuation.



Picture Type: Photo Caption: Picture 4. EEG atlas: localization-related epilepsies. Sharp waves, left temporal region. The maximum (phase reversal) is at F7 and T1. The small sharp wave that follows would not be sufficient in itself owing to its small amplitude, but in the context of other definite ones, is most likely significant.



Picture Type: Photo Caption: Picture 5. EEG atlas: localization-related epilepsies. Sharp wave, left temporal region. The sharp wave is, like most significant epileptiform discharges, followed by slowing and “disruption” of the background. The referential montage (right panel) confirms that the maximum is at electrode T2, followed by F8 and T4.





Picture Type: Photo Caption: Picture 6. EEG atlas: localization-related epilepsies. Spike, left frontal region. Note the typical aftergoing slow wave. The referential montage (right panel) shows that the maximum is at Fp1 and F7 about equally, followed by F3.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 7. EEG atlas: localization-related epilepsies. EEG seizure, left temporal region. This is characterized by a rhythmic discharge with “build-up” (ie, evolution in frequency and amplitude).



Picture Type: Photo Caption: Picture 8. PowerPoint presentation of Images 1-7.


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Benbadis SR: Observations on the misdiagnosis of generalized epilepsy as partial epilepsy: causes and consequences. Seizure 1999 May; 8(3): 140-5[Medline]. Benbadis SR, Luders HO: Epileptic syndromes: an underutilized concept. Epilepsia 1996 Nov; 37(11): 1029-34[Medline]. Benbadis SR, Tatum WO, Vale FL: When drugs don't work: an algorithmic approach to medically intractable epilepsy. Neurology 2000 Dec 26; 55(12): 1780-4[Medline]. Benbadis SR, Wyllie E: Pediatric epilepsy syndromes. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:468-480. Benbadis SR, Wyllie E, Bingaman W: Intracranial EEG and localization studies. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:1067-1075. Cascino GD, Hulihan JF, Sharbrough FW, et al: Parietal lobe lesional epilepsy: electroclinical correlation and operative outcome. Epilepsia 1993 May-Jun; 34(3): 522-7[Medline]. Cascino GD, Trenerry MR, So EL, et al: Routine EEG and temporal lobe epilepsy: relation to long-term EEG monitoring, quantitative MRI, and operative outcome. Epilepsia 1996 Jul; 37(7): 651-6[Medline]. Engel J Jr: Surgery for seizures. N Engl J Med 1996 Mar 7; 334(10): 647-52[Medline].


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Engel J Jr: Classifications of the International League Against Epilepsy: time for reappraisal. Epilepsia 1998 Sep; 39(9): 10147[Medline]. Gastaut H: A new type of epilepsy: benign partial epilepsy of childhood with occipital spike-waves. Clin Electroencephalogr 1982 Jan; 13(1): 13-22[Medline]. International League Against Epilepsy, Commission on Classification & Terminolog: Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989 Jul-Aug; 30(4): 389-99[Medline]. Kuzniecky R, Burgard S, Faught E, et al: Predictive value of magnetic resonance imaging in temporal lobe epilepsy surgery. Arch Neurol 1993 Jan; 50(1): 65-9[Medline]. Kuzniecky RI: Magnetic resonance imaging in developmental disorders of the cerebral cortex. Epilepsia 1994; 35 Suppl 6: S4456[Medline]. Laskowitz DT, Sperling MR, French JA, et al: The syndrome of frontal lobe epilepsy: characteristics and surgical management. Neurology 1995 Apr; 45(4): 780-7[Medline]. Levin KH, Lüders HO: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000. Loiseau P, Beaussart M: The seizures of benign childhood epilepsy with Rolandic paroxysmal discharges. Epilepsia 1973 Dec; 14(4): 381-9[Medline]. Lombroso CT: Sylvian seizures and midtemporal spike foci in children. Arch Neurol 1967 Jul; 17(1): 52-9[Medline]. Lüders H, Lesser RP, Dinner DS, et al: Benign focal epilepsy of childhood. In: Lüders H, Lesser RP, eds. Epilepsy: Eectroclinical Sndromes. London: Springer-Verlag; 1987:303-346. Lüders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000. Oldani A, Zucconi M, Asselta R, et al: Autosomal dominant nocturnal frontal lobe epilepsy. A video- polysomnographic and genetic appraisal of 40 patients and delineation of the epileptic syndrome. Brain 1998 Feb; 121 ( Pt 2): 205-23[Medline]. Risinger MW: Electroencephalographic strategies for determining the epileptogenic zone. In: Lüders, ed. Epilepsy Surgery. NY: Raven Press; 1992:337-347. Salanova V, Andermann F, Olivier A, et al: Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1930 and 1991. Surgery of occipital lobe epilepsy. Brain 1992 Dec; 115 ( Pt 6): 1655-80[Medline]. Salanova V, Andermann F, Rasmussen T, et al: Parietal lobe epilepsy. Clinical manifestations and outcome in 82 patients treated surgically between 1929 and 1988. Brain 1995 Jun; 118 ( Pt 3): 607-27[Medline]. Scheffer IE, Bhatia KP, Lopes-Cendes I, et al: Autosomal dominant nocturnal frontal lobe epilepsy. A distinctive clinical disorder. Brain 1995 Feb; 118 ( Pt 1): 61-73[Medline]. Tich SN, Pereon Y: Semiological seizure classification. Epilepsia 1999 Apr; 40(4): 531[Medline]. Wyllie E: EEG atlas. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001.


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eMedicine - EEG Atlas: Normal Awake EEG : Article by Selim R Benbadis, MD


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Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida


CME available for this topic. Click here to take this CME.

Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Patient Education Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Paul E Barkhaus, MD, Director, Division of Neuromuscular Diseases, Milwaukee Veterans Administration Medical Center; Professor, Department of Neurology, Medical College of Wisconsin; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

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This article describes the most common features of the normal awake EEG. The images at the end of the article show representative examples of the features discussed here. The alpha rhythm is the most prominent feature of the normal mature EEG. It typically is identified first during the review. Beta activity refers to a frequency band rather than a distinct (specific) rhythm such as alpha or mu. Beta activity is commonly present in the EEG of healthy people. However, it is often difficult to see because of its low amplitude. Gastaut initially described the mu rhythm in 1952. This morphologically distinct activity is observed in approximately 17-19% of young adults. WAVEFORM DESCRIPTION

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eMedicine - EEG Atlas: Normal Awake EEG : Article by Selim R Benbadis, MD Author Information Introduction Waveform Description Clinical Correlation Pictures Bibliography

Alpha rhythm The normal alpha rhythm has the following characteristics: ●

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Frequency of 8-12 Hz - Lower limit of normal generally accepted in adults and children older than 8 years is 8 Hz Location - Posterior dominant; occasionally, the maximum may be a little more anterior, and it may be more widespread

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Morphology - Rhythmic, regular, and waxing and waning

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Amplitude - Generally 20-100 mV

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Reactivity - Best seen with eyes closed; attenuates with eye opening

Beta activity Normal beta activity has the following characteristics: ●

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Frequency (by definition) greater than 13 Hz - Common 18-25 Hz, less common 14-16 Hz, and rare 3540 Hz Location - Mostly frontocentral but somewhat variable; some describe various types according to location and reactivity: generalized, precentral, and posterior

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Morphology - Usually rhythmic, waxing and waning, and symmetric

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Amplitude - Usually range of 5-20 mV

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Reactivity - Most common 18- to 25-Hz beta activity enhanced during stages I and II sleep and tends to decrease during deeper sleep stages; central beta activity may be reactive (attenuates) to voluntary movements and proprioceptive stimuli; in infants older than 6 months, onset of sleep marked by increased beta activity in central and postcentral regions

Mu rhythm Characteristics of the mu rhythms are as follows: ●

Frequency of 7-11 Hz - Generally in alpha frequency band (8-12 Hz)

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Location - Centroparietal area

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Morphology - Archlike shape or like an "m"; most often asymmetric and asynchronous between the 2 sides and may be unilateral Amplitude - Generally low to medium and comparable to that of the alpha rhythm Reactivity - Most characteristic feature defining the mu rhythm; mu rhythm attenuates with contralateral extremity movement, the thought of a movement, or tactile stimulation; contrary to the alpha rhythm, does not react to eye opening and closing

The mu rhythm has been documented on subdural recording of both sensory and motor cortex and shows the same characteristics as that seen on surface EEG, including distribution, morphology, and reactivity. Furthermore, some correspondence exists between functional mapping of sensorimotor function and



somatotopic distribution of mu reactivity. CLINICAL CORRELATION

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Alpha rhythm Occasionally the alpha rhythm is of very low amplitude or even not identifiable. This is not abnormal. In addition to amplitude, other characteristics can vary somewhat without being abnormal, including morphology (eg, spiky), distribution (eg, widespread), and harmonic frequency (eg, slow or fast alpha variant). Beta activity In healthy individuals, beta activity commonly can be mildly different (<35%) in amplitude between the 2 hemispheres, which may be caused by differences in skull thickness. Definite focal, regional, or hemispheric difference (at least 50%) in amplitude may be significant and may suggest either skull defect (side with higher amplitude) or a structural lesion (side with lower amplitude). The amount and voltage of beta activity is enhanced by commonly used sedative medications (benzodiazepines, barbiturates). Mu rhythm Asymmetry, unilaterality, or asynchrony of the mu rhythm is generally not abnormal unless associated with other abnormalities. Very-high-voltage mu activity may be recorded in the central regions over skull defects and may become sharp in configuration, and thus can be mistaken for epileptiform discharges. When mu rhythm is detected in an EEG, it should be verified by testing its reactivity. PICTURES

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Caption: Picture 1. EEG atlas: normal awake EEG. A 10-second segment showing a well-formed and wellregulated alpha rhythm at 9 Hz. Note that it is very regular, rhythmic, waxing and waning, and posterior dominant. The contrast between the first and second halves of the page illustrates the reactivity of a normal alpha rhythm, with attenuation upon eye opening.



Picture Type: Photo Caption: Picture 2. EEG atlas: normal awake EEG. Fleeting alpha. At times, as shown here, the alpha rhythm can be identified only in very brief bursts and often immediately after eye closure. If normal in frequency, this is normal.





Picture Type: Photo Caption: Picture 3. EEG atlas: normal awake EEG. This is an example of an alpha rhythm with a wider distribution than is typical. If frequency and reactivity are normal, this is another variation of normal. A similar EEG pattern can be seen in patients in a coma (ie, alpha coma), but in these situations it is usually unreactive.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: normal awake EEG. This is an example of "slow alpha variant." The patient's alpha rhythm at 12 Hz is seen in the second half of the sample. The first half shows a subharmonic at half that frequency, and this is the "slow alpha variant."


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 5. EEG atlas: normal awake EEG. A sample of awake EEG showing the normal or usual amount of beta activity. As shown here, beta activity is often easier to identify during relaxed wakefulness or early drowsiness.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: normal awake EEG. Mu rhythm over the left (greater than right) central region. To be absolutely certain that this is a mu rhythm, reactivity should be tested. However, morphology (not absolutely typical but fairly so), frequency, and distribution strongly suggest that this is a mu rhythm.




eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 7. EEG atlas: normal awake EEG. An example of a typical normal alpha rhythm, showing clear attenuation upon eye opening (second half of page)



Picture Type: Photo Caption: Picture 8. EEG atlas: normal awake EEG. This is the normal amount of beta activity, frontally predominant, with waxing and waning amplitude.



Picture Type: Photo Caption: Picture 9. EEG atlas: normal awake EEG. Alpha rhythm with somewhat "spiky" or sharply contoured morphology. When fragmented (eg, in drowsiness), this can be misinterpreted as sharp waves.



Picture Type: Photo BIBLIOGRAPHY

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Arroyo S, Lesser RP, Gordon B, et al: Functional significance of the mu rhythm of human cortex: an electrophysiologic study with subdural electrodes. Electroencephalogr Clin Neurophysiol 1993 Sep; 87(3): 76-87[Medline]. Benbadis SR: Focal disturbances of brain function. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology.



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Philadelphia: WB Saunders Co; 2000:457-467. McFarland DJ, Miner LA, Vaughan TM, et al: Mu and beta rhythm topographies during motor imagery and actual movements. Brain Topogr 2000 Spring; 12(3): 177-86[Medline]. Pfurtscheller G, Stancak A Jr, Edlinger G: On the existence of different types of central beta rhythms below 30 Hz. Electroencephalogr Clin Neurophysiol 1997 Apr; 102(4): 316-25[Medline]. Pfurtscheller G, Neuper C, Krausz G: Functional dissociation of lower and upper frequency mu rhythms in relation to voluntary limb movement. Clin Neurophysiol 2000 Oct; 111(10): 1873-9[Medline]. Pineda JA, Allison BZ, Vankov A: The effects of self-movement, observation, and imagination on mu rhythms and readiness potentials (RP's): toward a brain-computer interface (BCI). IEEE Trans Rehabil Eng 2000 Jun; 8(2): 219-22[Medline].


EEG Atlas: Normal Awake EEG excerpt



eMedicine - EEG Atlas: Normal Sleep EEG - Rapid Eye Movement Sleep : Article by Selim R Benbadis, MD


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EEG Atlas: Normal Sleep EEG Rapid Eye Movement Sleep

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Synonyms and related keywords: EEG desynchronization, REM sleep, saw tooth wave AUTHOR INFORMATION

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Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early 1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in 2 broad types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time. REM sleep normally is not seen on routine EEGs, because the normal latency to REM sleep (100 min) is well beyond the duration of routine EEG recordings (approximately 20-30 min). The appearance of REM sleep during a routine EEG is referred to as sleep-onset REM period (SOREMP) and is considered an abnormality. While not observed on routine EEG, REM sleep commonly is seen during prolonged (>24 h) EEG monitoring. Representative examples of waveforms described here can be seen in the images at the end of this article.





WAVEFORM DESCRIPTIONS

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By strict sleep staging criteria on polysomnography, REM sleep is defined by (1) rapid eye movements; (2) muscle atonia; and (3) EEG “desynchronization” (compared to slow wave sleep). Thus, 2 of the 3 defining characteristics are not cerebral waves and theoretically require monitoring of eye movements (electrooculogram [EOG]) and muscle tone (electromyelogram [EMG]). Fortunately, muscle activity and eye movements can be evaluated on EEG, thus REM sleep is usually not difficult to identify. In addition to the 3 features already named, “saw tooth” waves also are seen in REM sleep. ●

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EEG desynchronization: The EEG background activity changes from that seen in slow wave sleep (stage III or IV) to faster and lower voltage activity (theta and beta), resembling wakefulness. Saw tooth waves are a special type of central theta activity that has a notched morphology resembling the blade of a saw and usually occurs close to rapid eye movements (ie, phasic REM). They are only rarely clearly identifiable. Rapid eye movements: These are saccadic, predominantly horizontal, and occur in repetitive bursts.

Despite the lack of a dedicated EMG channel, the muscle atonia that characterizes REM sleep is usually apparent as a general sense of “quiet” muscle artifacts compared to wakefulness. CLINICAL CORRELATION

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The duration of REM sleep increases progressively with each cycle and tends to predominate late in the sleep period into early morning. The occurrence of REM too soon after sleep onset, referred to as SOREMP, is considered pathological. However, newborns and infants enter REM more rapidly and spend a higher proportion of sleep in REM (this is true in most species and supports the theory that REM sleep is involved in brain development). PICTURES

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Caption: Picture 1. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. REM sleep with rapid (saccadic) eye movements. While muscle “atonia” cannot be proven without a dedicated electromyogram (EMG) channel, certainly EMG artifact is absent with a “quiet” recording. Also, no alpha rhythm is present that would suggest wakefulness.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. Typical saccadic eye movements of REM sleep are shown, with lateral rectus “spikes” seen just preceding the lateral abducting eye movements.





Picture Type: Photo Caption: Picture 3. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. In addition to rapid eye movements, this REM sleep record is characterized by brief fragments of alpha rhythm (first half) and central saw tooth waves (second half).


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This is a good example of saw tooth waves seen in REM sleep and their “notched” morphology.



Picture Type: Photo Caption: Picture 5. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This is a good example of saw tooth waves seen in REM sleep and their “notched” morphology, best seen here in the Cz-Pz (last) channel.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This illustrates the typical appearance of saw tooth waves on a polysomnogram (PSG) display, equivalent to 1 cm/s.





Picture Type: Photo Caption: Picture 7. EEG atlas: normal sleep EEG – rapid eye movement sleep. PowerPoint presentation of pictures 1-6


Section 6 of 6


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Aserinsky E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10. Benbadis SR, Wolgamuth BR, Perry MC, et al: Dreams and rapid eye movement sleep in the multiple sleep latency test. Sleep 1995 Feb; 18(2): 105-8[Medline]. Chockroverty S: An overview of sleep. In: Chokroverty S, ed. Sleep Disorder Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:7-20. Dement W, Kleitman N: Cyclic variations of EEG during sleep and their relation to eye movements, body motility and dreaming. Electroencephalogr Clin Neurophysiol 1957; 9: 673-690. Loomis AL, Harvey EN, Hobart GA: Potential rhythms of the cerebral cortex during sleep. Science 1935; 81: 597-598. Loomis AL, Harvey EN, Hobart GA: Brain potentials during hypnosis. Science 1936; 83: 239-241. Loomis AL, Harvey EN, Hobart GA: Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21: 127144. Loomis AL, Harvey EN, Hobart G: Distribution of disturbance patterns in the human electroencephalogram with special reference to sleep. J Neurophysiol 1938; 1: 413-430. Reynolds CF 3rd, Kupfer DJ, Taska LS, et al: EEG sleep in elderly depressed, demented, and healthy subjects. Biol Psychiatry 1985 Apr; 20(4): 431-42[Medline]. Sakai T, Kohsaka S, Kohsaka M: Functional changes of the brainstem triggering vertex sharp wave with spindle. Psychiatry Clin Neurosci 1999 Apr; 53(2): 167-9[Medline]. Steriade M: Neurophysiological mechanism of non-rapid eye movement (resting) sleep. In: Chokroverty S, ed. Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:51-62. Vignaendra V, Matthews RL, Chatrian GE: Positive occipital sharp transients of sleep: relationships to nocturnal sleep cycle in man. Electroencephalogr Clin Neurophysiol 1974 Sep; 37(3): 239-46[Medline].


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eMedicine - EEG Atlas: Normal Sleep EEG - Stage I : Article by Selim R Benbadis, MD


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EEG Atlas: Normal Sleep EEG Stage I

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Synonyms and related keywords: drowsiness, presleep, sleep stages AUTHOR INFORMATION

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Section 2 of 6


Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early 1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in two broad types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time. Stage I sleep also is referred to as drowsiness or presleep and is the first or earliest stage of sleep. Representative EEG waveforms are shown in the images at the end of this article.


Section 3 of 6




eMedicine - EEG Atlas: Normal Sleep EEG - Stage I : Article by Selim R Benbadis, MD Author Information Introduction Waveform Descriptions Clinical Correlation Pictures Bibliography

The features of drowsiness are as follows: ●

Slow rolling eye movements (SREMs)

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Attenuation (drop out) of the alpha rhythm

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Central or frontocentral theta activity

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Enhanced beta activity

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Positive occipital sharp transients of sleep (POSTS)

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Vertex sharp transients

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Hypnagogic hypersynchrony

Slow rolling eye movements SREMs are usually the first evidence of drowsiness seen on the EEG. SREMs of drowsiness most often are horizontal but can be vertical or oblique, and their distribution is similar to eye movements in general (see EEG Atlas: EEG Artifacts). However, they are slow (ie, typically 0.25-0.5 Hz). SREMs disappear in stage II and deeper sleep stages. Alpha dropout Drop out of alpha activity typically occurs together with or nearby SREM. The alpha rhythm gradually becomes slower, less prominent, and fragmented. Positive occipital sharp transients of sleep POSTS start to occur in healthy people at age 4 years, become fairly common by age 15 years, remain common through age 35 years, and start to disappear by age 50 years. POSTS are seen very commonly on EEG and have been said to be more common during daytime naps than during nocturnal sleep. Most characteristics of POSTS are contained in their name. They have a positive maximum at the occiput, are contoured sharply, and occur in early sleep (stages I and II). Their morphology classically is described as "reverse check mark," and their amplitude is 50-100 µV. They typically occur in runs of 4-5 Hz and are bisynchronous, although they may be asymmetric. They persist in stage II sleep but usually disappear in subsequent stages. Vertex sharp transients Also called vertex waves or V waves, these transients are almost universal. Although they often are grouped together with K complexes, strictly speaking, vertex sharp transients are distinct from K complexes. Like K complexes, vertex waves are maximum at the vertex (central midline placement of electrodes [Cz]), so that, depending on the montage, they may be seen on both sides, usually symmetrically. Their amplitude is 50-150 µV. They can be contoured sharply and occur in repetitive runs, especially in children. They persist in stage II sleep but usually disappear in subsequent stages. Unlike K complexes, vertex waves are narrower and more focal and by themselves do not define stage II. Hypnagogic hypersynchrony Hypnagogic hypersynchrony (first described by Gibbs and Gibbs, 1950) is a well-recognized normal variant of drowsiness in children aged 3 months to 13 years. This is described as paroxysmal bursts (3-5 Hz) of highvoltage (as high as 350 µV) sinusoidal waves, maximally expressed in the prefrontal-central areas, that brake after the cerebral activity amplitude drops during drowsiness.




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The importance of normal sleep patterns is that they should not be mistaken for pathologic sharp waves. Several normal stage I patterns easily can be mistaken for epileptic sharp waves or spikes, including vertex sharp transients, POSTS, and even fragments of alpha rhythm as it drops out. PICTURES

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Caption: Picture 1. EEG atlas: normal sleep EEG - stage I. The earliest indication of transition from wakefulness to stage I sleep (drowsiness) is shown here and usually consists of a combination of (1) drop out of alpha activity and (2) slow rolling eye movements.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 2. EEG atlas: normal sleep EEG - stage I. Slow rolling (lateral) eye movements during stage I sleep. Like faster lateral eye movements, slow ones are best seen at the F7 and F8 electrodes, with the corneal positivity indicating the side of gaze.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: normal sleep EEG - stage I. On this transverse montage, typical vertex sharp transients are seen. In contrast to K complexes, these are narrow (brief) and more focal, with a maximum negativity at the mid line (Cz and to a lesser degree Fz). These are seen in sleep stages I and II.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 4. EEG atlas: normal sleep EEG - stage I. Vertex waves are focal sharp transients typically best seen on transverse montages (through the midline) and would be missed on this longitudinal bipolar montage if it did not include midline channels (Fz-Cz-Pz). Vertex waves are seen in sleep stages I and II.





Picture Type: Photo Caption: Picture 5. EEG atlas: normal sleep EEG - stage I. Positive occipital sharp transients of sleep (POSTS) are seen in both occipital regions, with their typical characteristics contained in their name. They also have morphology classically described as “reverse check mark” and often occur in consecutive runs of several seconds, as shown here.


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: normal sleep EEG - stage I. PowerPoint presentation of Images 1-5.


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Aserinski E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10. Benbadis SR, Perry MC, Wolgamuth BR, et al: The multiple sleep latency test: comparison of sleep onset criteria. Sleep 1996 Oct; 19(8): 632-6[Medline]. Chatrian GE, White LE Jr, Daly D: Electroencephalographic patterns resembling those of sleep in certain comatose states after injuries to the head. Electroencephalogr Clin Neurolphysiol 1963; 15: 272-280. Chockroverty S: An overview of sleep. In: Chokroverty S, ed. Sleep Disorder Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:7-20. Dement W, Kleitman N: Cyclic variations of EEG during sleep and their relation to eye movements, body motility and dreaming. Electroencephalogr Clin Neurophysiol 1957; 9: 673-690. Gibbs FA, Gibbs EL: Atlas of Electroencephalography. Normal Controls. Vol 1. Cambridge, Mass: Addison-Wesley; 1950. Loomis AL, Harvey EN, Hobart GA: Potential rhythms of the cerebral cortex during sleep. Science 1935; 81: 597-598. Loomis AL, Harvey EN, Hobart GA: Brain potentials during hypnosis. Science 1936; 83: 239-241. Loomis AL, Harvey EN, Hobart GA: Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21: 127144. Loomis AL, Harvey EN, Hobart G: Distribution of disturbance patterns in the human electroencephalogram with special reference to sleep. J Neurophysiol 1938; 1: 413-430. Reynolds CF 3rd, Kupfer DJ, Taska LS, et al: EEG sleep in elderly depressed, demented, and healthy subjects. Biol Psychiatry 1985 Apr; 20(4): 431-42[Medline]. Sakai T, Kohsaka S, Kohsaka M: Functional changes of the brainstem triggering vertex sharp wave with spindle. Psychiatry Clin Neurosci 1999 Apr; 53(2): 167-9[Medline]. Steriade M: Neurophysiological mechanism of non-rapid eye movement (resting) sleep. In: Chokroverty S, ed. Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:51-62. Vignaendra V, Matthews RL, Chatrian GE: Positive occipital sharp transients of sleep: relationships to nocturnal sleep cycle in man. Electroencephalogr Clin Neurophysiol 1974 Sep; 37(3): 239-46[Medline].

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eMedicine - EEG Atlas: Normal Sleep EEG - Stage I : Article by Selim R Benbadis, MD Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

EEG Atlas: Normal Sleep EEG - Stage I excerpt



eMedicine - EEG Atlas: Normal Sleep EEG - Stage II : Article by Selim R Benbadis, MD


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Synonyms and related keywords: K complex, sleep spindle, sleep stages AUTHOR INFORMATION

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Continuing Education Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, University of South Florida Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Norberto Alvarez, MD, Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston Children's Hospital, Harvard Medical School; Paul E Barkhaus, MD, Director, Division of Neuromuscular Diseases, Milwaukee Veterans Administration Medical Center; Professor, Department of Neurology, Medical College of Wisconsin; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants INTRODUCTION

Section 2 of 6


Loomis provided the earliest detailed description of various stages of sleep in the mid 1930s, and in the early 1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in two broad types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time. Stage II is the predominant sleep stage during a normal night's sleep. The distinct and principal EEG criterion to establish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles is necessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the appearance of K complexes, but since K complexes typically are associated with a spindle, spindles are the





defining features of stage II sleep. Except for slow rolling eye movements, all patterns described under stage I persist in stage II sleep (see EEG Atlas: Normal Sleep EEG – Stage I). Representative examples of the waveforms described here are shown in the images at the end of this article.


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Sleep spindles normally first appear in infants aged 6-8 weeks and are bilaterally asynchronous. These become well-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles have a frequency of 12-16 Hz (typically 14 Hz) and are maximal in the central region (vertex), although they occasionally predominate in the frontal regions. They occur in short bursts of waxing and waning spindlelike (fusiform) rhythmic activity. Amplitude is usually 20-100 µV. Extreme spindles (described by Gibbs and Gibbs) are unusually high-voltage (100-400 µV) and prolonged (>20 s) spindles located over the frontal regions. K complexes (initially described by Loomis) are high amplitude (>100 µV), broad (>200 ms), diphasic, and transient and often are associated with sleep spindles. Location is frontocentral, with a typical maximum at the midline (central midline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). They occur spontaneously and are elicited as an arousal response. They may have an association with blood pressure fluctuation during sleep. CLINICAL CORRELATION

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The stigmata of stage II sleep, spindles and K complexes, are usually easy to identify and are less subject to overinterpretation or misinterpretation than the patterns of stage I sleep. PICTURES

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Caption: Picture 1. EEG atlas: normal sleep EEG - stage II. PowerPoint presentation.

Click to see detail Picture Type: Presentation Caption: Picture 2. EEG atlas: normal sleep EEG – stage II. This shows a K complex, typically a highamplitude long-duration biphasic waveform with overriding spindle. This is a transverse montage, which shows the typical maximum (manifested by a "phase reversal") at the midline.



Picture Type: Photo Caption: Picture 3. EEG atlas: normal sleep EEG – stage II. Typical sleep spindles with short-lived waxing and waning 15-Hz activity maximum in the frontocentral regions. Note the associated slow (theta) activity that also characterizes stage II sleep.





Picture Type: Photo Caption: Picture 4. EEG atlas: normal sleep EEG – stage II. Vertex sharp transients. This transverse montage illustrates the maximum negativity (manifested by a negative phase reversal) at the midline. The location is similar to that of K complexes, but these are shorter (narrower) and more localized.



Picture Type: Photo Caption: Picture 5. EEG atlas: normal sleep EEG - stage II. K complex, with its typical characteristics: highamplitude, widespread, broad, diphasic slow transient with overriding spindle. On the longitudinal montage (left), the K complex appears to be generalized. However, the transverse montage clearly shows that the maximum (phase reversal) is at the midline (Fz and Cz).


eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 6. EEG atlas: normal sleep EEG - stage II. A mixture of spindles (ie, bicentral short-lived rhythmic 14 Hz bursts) and positive occipital sharp transients of sleep (POSTS) can be seen. POSTS occur in stage I, but the presence of spindles is “diagnostic” of stage II.


eMedicine Zoom View (Interactive!) Picture Type: ECG Caption: Picture 7. EEG atlas: normal sleep EEG - stage II. A mixture of positive occipital sharp transients of sleep (POSTS) and spindles (fronto-central short-lived rhythmic 14-Hz bursts) can be seen.





Picture Type: Photo BIBLIOGRAPHY

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Aserinsky E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10. Chatrian GE, White LE Jr, Daly D: Electroencephalographic patterns resembling those of sleep in certain comatose states after injuries to the head. Electroencephalogr Clin Neurolphysiol 1963; 15: 272-280. Chockroverty S: An overview of sleep. In: Chokroverty S, ed. Sleep Disorder Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:7-20. Cote KA, de Lugt DR, Langley SD, et al: Scalp topography of the auditory evoked K-complex in stage 2 and slow wave sleep. J Sleep Res 1999 Dec; 8(4): 263-72[Medline]. Dement W, Kleitman N: Cyclic variations of EEG during sleep and their relation to eye movements, body motility and dreaming. Electroencephalogr Clin Neurophysiol 1957; 9: 673-690. Gibbs EL, Gibbs FA: Extreme spindles: correlation of electroencephalographic sleep pattern with mental retardation. Science 1962; 138: 1106-1107. Hughes JR: Sleep spindles revisited. J Clin Neurophysiol 1985 Jan; 2(1): 37-44[Medline]. Jankel WR, Niedermeyer E: Sleep spindles. J Clin Neurophysiol 1985 Jan; 2(1): 1-35[Medline]. Loomis AL, Harvey EN, Hobart GA: Potential rhythms of the cerebral cortex during sleep. Science 1935; 81: 597-598. Loomis AL, Harvey EN, Hobart GA: Brain potentials during hypnosis. Science 1936; 83: 239-241. Loomis AL: Harvey EN and Hobart GA Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21: 127-144. Loomis AL, Harvey EN, Hobart G: Distribution of disturbance patterns in the human electroencephalogram with special reference to sleep. J Neurophysiol 1938; 1: 413-430. Monstad P, Guilleminault C: Cardiovascular changes associated with spontaneous and evoked K- complexes. Neurosci Lett 1999 Mar 26; 263(2-3): 211-3[Medline]. Naitoh P, Antony-Baas V, Muzet A, et al: Dynamic relation of sleep spindles and K-complexes to spontaneous phasic arousal in sleeping human subjects. Sleep 1982; 5(1): 58-72[Medline]. Sakai T, Kohsaka S, Kohsaka M: Functional changes of the brainstem triggering vertex sharp wave with spindle. Psychiatry Clin Neurosci 1999 Apr; 53(2): 167-9[Medline]. Steriade M: Neurophysiological mechanism of non-rapid eye movement (resting) sleep. In: Chokroverty S, ed. Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:51-62. Vignaendra V, Matthews RL, Chatrian GE: Positive occipital sharp transients of sleep: relationships to nocturnal sleep cycle in man. Electroencephalogr Clin Neurophysiol 1974 Sep; 37(3): 239-46[Medline].


EEG Atlas: Normal Sleep EEG - Stage II excerpt



eMedicine - EEG Atlas: Normal Sleep EEG - Stages III and IV : Article by Selim R Benbadis, MD


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EEG Atlas: Normal Sleep EEG Stages III and IV

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Synonyms and related keywords: delta sleep, delta waves, sleep stages, slow wave sleep, SWS AUTHOR INFORMATION

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Section 1 of 6





Section 2 of 6


Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early 1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in two broad types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time. Total sleep time in the healthy young adult approximates 7.5-8 hours. In the full-term newborn, sleep cycles last approximately 60 minutes (50% NREM, 50% REM, alternating through a 3-4 h interfeeding period). The newborn sleeps approximately 16-20 hours per day; these numbers decline to a mean of 10 hours during childhood.





Stages III and IV usually are grouped together as “slow wave sleep” or “delta sleep.” Slow wave sleep (SWS) usually is not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged (>24 h) EEG monitoring. Representative examples of SWS EEGs are shown in the images at the end of this article. Men aged 20-29 years spend about 21% of their total sleep in SWS, those aged 40-49 years spend about 8% in SWS, and those aged 60-69 spend about 2% in SWS (Williams et al, 1974). Notably, elderly people's sleep comprises only a small amount of deep sleep (virtually no stage IV sleep and scant stage III sleep). Their total sleep time approximates 6.5 hours. SWS is characterized by relative body immobility, although body movement artifacts may be registered on electromyogram (EMG) toward the end of SWS. WAVEFORM DESCRIPTIONS

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SWS, or delta sleep, is characterized, as the name implies, by delta activity. This typically is generalized and polymorphic or semirhythmic. By strict sleep staging criteria on polysomnography, SWS is defined by the presence of such delta activity for more than 20% of the time, and an amplitude criterion of at least 75 µV often is applied. The distinction between stages III and IV is only a quantitative one that has to do with the amount of delta activity. Stage III is defined by delta activity that occupies 20-50% of the time, whereas in stage IV delta activity represents greater than 50% of the time. Sleep spindles and K complexes may persist in stage III and even to some degree in stage IV, but they are not prominent. CLINICAL CORRELATION

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As mentioned above, SWS usually is not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged EEG monitoring. One important clinical aspect of SWS is that certain parasomnias occur specifically out of this stage and must be differentiated from seizures. These “slow wave sleep parasomnias” include confusional arousals, night terrors (pavor nocturnus), and sleep walking (somnambulism). PICTURES

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Caption: Picture 1. EEG atlas: normal sleep EEG – stages III and IV. Slow wave sleep with predominantly delta activity, especially in the first half.



Picture Type: Photo Caption: Picture 2. EEG atlas: normal sleep EEG – stages III and IV. Slow wave sleep with predominantly delta activity.




eMedicine Zoom View (Interactive!) Picture Type: Photo Caption: Picture 3. EEG atlas: normal sleep EEG – stages III and IV. PowerPoint presentation of pictures 1-2


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Aserinski E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10. Chatrian GE, White LE Jr, Daly D: Electroencephalographic patterns resembling those of sleep in certain comatose states after injuries to the head. Electroencephalogr Clin Neurolphysiol 1963; 15: 272-280. Chockroverty S: An overview of sleep. In: Chokroverty S, ed. Sleep Disorder Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:7-20. Daly DD, Pedley TA: Current Practice of Clinical Practice of Electroencephalography. 2nd ed. New York: Raven Press; 1990: 574575. Dement W, Kleitman N: Cyclic variations of EEG during sleep and their relation to eye movements, body motility and dreaming. Electroencephalogr Clin Neurophysiol 1957; 9: 673-690. Loomis AL, Harvey EN, Hobart GA: Potential rhythms of the cerebral cortex during sleep. Science 1935; 81: 597-598. Loomis AL, Harvey EN, Hobart GA: Brain potentials during hypnosis. Science 1936; 83: 239-241. Loomis AL, Harvey EN, Hobart GA: Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21: 127144. Loomis AL, Harvey EN, Hobart G: Distribution of disturbance patterns in the human electroencephalogram with special reference to sleep. J Neurophysiol 1938; 1: 413-430. Reynolds CF 3rd, Kupfer DJ, Taska LS, et al: EEG sleep in elderly depressed, demented, and healthy subjects. Biol Psychiatry 1985 Apr; 20(4): 431-42[Medline]. Steriade M: Neurophysiological mechanism of non-rapid eye movement (resting) sleep. In: Chokroverty S, ed. Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:51-62. Williams RL, Karacan I, Hursch CJ: EEG of Human Sleep: Clinical Applications. New York: John Wiley & Sons; 1974.


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