This action might not be possible to undo. Are you sure you want to continue?
EEG in Dementia and Encephalopathy: …
eMedicine Specialties > Neurology > Electroencephalography and Evoked Potentials
EEG in Dementia and Encephalopathy
Eli S Neim an, DO, Assistant Professor of Neurology, Seton Hall University School of Graduate Medical Education, Comprehensive Epilepsy Center, New Jersey Neuroscience Institute-JFK Medical Center, Edison, NJ Philip A Hanna, MD, Associate Professor, Department of Neuroscience, Seton Hall University School of Graduate Medical Education; Residency Program Director, New Jersey Neuroscience Institute, JFK Medical Center; Neurology Director, Huntington's Disease Unit, JFK Hartw yck-Cedarbrook Updated: Nov 11, 2009
EEG has been employed clinically for some time as a measure of brain function in the hope of determining and differentiating certain functional conditions of the brain. It is used in patients with cognitive dysfunction, either a general decline of overall brain function or a localized or lateralized deficit. This article primarily addresses the clinical use of EEG in evaluation of dementias and encephalopathies. In addition, aspects of digital EEG and other newer developments are discussed briefly at the end of the article. Definition of dementia Criteria from Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) should be used in the diagnosis of dementia. Clinical dementia is a fairly broad-based decline of brain function; most definitions center on the patient's intellectual decline and memory dysfunction. This is, however, a fairly simplistic approach; dementia encompasses much more than these fundamental deficits. Many of the dementias have distinguishing features. The process that constitutes normal aging is still an ongoing debate. As our understanding and testing procedures develop, more people are being classified as suffering from some type of dementia. In 1998, Widagdo et al performed a quantitative EEG (QEEG) study of age-related changes during cognitive tasks.[1 ]This study revealed no conclusive differences between the young and the elderly. Cognitive decline, unlike normal aging, is associated with alterations in the temporospatial characteristics of EEG. The diagnosis of the initial stages of dementia is based mainly on neuropsychological testing and clinical suspicion. The EEG findings are nonspecific, as shown below).
EEG in Dementia and Encephalopathy: …
EEG in dementia.
EEG findings in dementia In early dementia, the resting alpha frequency declines. Most authors agree that the lower limit of normal alpha frequency is 8 cycles per second. Medications can slow the posterior dominant rhythm; therefore, medication effect should always be excluded. In assessing the frequency of the alpha rhythm, alerting maneuvers are essential in order to ensure that the patient is in the best awake state and not drowsy. Computerized methods, such as EEG spectral analysis, coherence, and complexity (ie, correlation dimension), have been demonstrated to correspond to cognitive function. Stevens et al recorded EEGs during 2 resting conditions (eyes closed and eyes opened) and 2 tasks (mental arithmetic and a lexical decision). The goal of the study was to evaluate which temporal and spatial EEG descriptors change with cognitive decline and normal aging. The EEGs were analyzed by using EEG microstates. The primary findings were a significant increase in the number of ultrashort EEG microstates and a reduction in the average duration of EEG microstates in cognitively impaired and demented patients. Cognitive impairment was associated with a reduction or loss of EEG reactivity. In contrast, no alterations in temporal or spatial EEG descriptors were found in normal aging. Cognitive tasks did not add to the information already obtained
07/12/2010 EEG in Dementia and Encephalopathy: … during the resting states. The reduction in EEG microstate duration correlated with loss of cognitive function. [2 ]
Therefore, temporospatial analysis of the EEG record is a useful indicator of cortical dysfunction in dementia and correlates with degree of cognitive impairment. Apparently, temporospatial analysis may be useful in distinguishing patients with dementia from those experiencing normal aging. These data are largely preliminary; whether they contribute additional information to the clinical data in evaluating dementia is unclear. Definition of encephalopathy Encephalopathy represents a brain state in which normal functioning of the brain is disturbed temporarily or permanently. Encephalopathy encompasses a number of conditions that lead to cognitive dysfunction. Some of these conditions are multifactorial and some have an established cause, such as hepatic or uremic encephalopathy. Because the EEG patterns in most dementias and encephalopathies demonstrate few specific features, they are discussed together. Some notable exceptions include Creutzfeldt-Jakob disease (CJD) and subacute sclerosing panencephalitis (SSPE); however, no specific patterns exist for most dementias and encephalopathies. Other conditions, such as hepatic and renal encephalopathies, carry distinguishing features; nevertheless, similar patterns may be seen in a fairly wide range of illnesses under certain conditions. EEG findings in encephalopathy In general, the most prominent feature of the EEG record in encephalopathies (if there is a change) is slowing of the normal background frequency. Over the course of the disease if serial EEGs are performed, disorganization of the record may develop gradually. Reactivity to photic or other type of external stimulation may be altered. If a QEEG is performed, it may show a frequency shift or decreased interhemispheric coherence of background frequencies. Some conditions are associated with an increase in seizure frequency, and in such cases, epileptic activity may be recorded. In a given context, the EEG can play a clinically useful role, especially since functional MRI, positron emission tomography (PET), and single-photon emission computed tomography (SPECT) are either still in an experimental stage or require special settings not widely available. Use of digital EEG data Although in the following sections digital EEG data are cited frequently, these data represent primarily digital analysis of clinical EEG recording. The referenced data are presumed to be based on an EEG recording that is read by a clinician; presently, it is recorded by using computerized technology for ease and also for availability for further analysis. A variety of mathematical transforms are available after the initial clinical interpretation—for example, coherence, Fourier transform, wavelets, and microstates (see Digital EEG). These allow for further comparisons with norms and control groups but should be interpreted in conjunction with the primary EEG reading.
Alzheimer disease EEG is the only clinical diagnostic instrument directly reflecting cortical neuronal functioning. Although the EEG may be normal or minimally disturbed in a number of patients in the initial stages of Alzheimer disease (AD), an abnormal EEG usually is recorded later in the course. A large percentage of patients with moderately severe to severe AD exhibit abnormal EEGs. In 1981, Stigsby reported diffuse increases of delta and theta frequencies, as well as decreases in the alpha and beta frequency ranges in AD. Frontal slowing was also seen with slowing more prominent anterior to the sylvian fissure, while the blood flow was more decreased posterior to the sylvian fissure. These findings may be explained by the fact that the EEG reflects the functional decline of the anterior structures, while the flow decrease correlates more with the structural damage of the parietal lobe. The frontal slowing probably reflects the loss of functioning of the frontal cholinergic system. [3 ] Wada et al showed that EEG coherence provides a measure of functional correlation between 2 EEG signals. They examined intrahemispheric EEG coherence at rest and during photic stimulation in 10 patients with dementia of the Alzheimer type. In the resting EEG, patients with AD had significantly lower coherence than gender and age-matched healthy control subjects in the alpha-1, alpha-2, and beta-1 frequency bands. EEG analysis during photic stimulation demonstrated that the patients had significantly lower coherence irrespective of the stimulus frequency. The changes in coherence from the resting state to the stimulus condition showed significant group differences in the region of the brain primarily involved in visual functioning. The patients had significantly lower coherence of their EEG reactivity to photic stimulation at 5 and 15 Hz over the posterior head regions. [4 ] These findings suggest that patients with AD may have an impairment of interhemispheric functional connectivity in both nonstimulus and stimulus conditions. This suggests a failure of normal stimulation-related brain activation in AD. Jelic et al found a positive correlation between levels of tau protein in the cerebrospinal fluid (CSF) and EEG alpha/delta ratio. In a subgroup with
07/12/2010 EEG in Dementia and Encephalopathy: … high CSF tau levels, a strong relationship between EEG alpha/theta and alpha/delta power was found. No such correlation was found in healthy controls and mildly cognitively impaired individuals with elevated CSF tau levels. [5 ]
Locatelli et al used EEG coherence to evaluate the functionality of cortical connections and to get information about the synchronization of the regional cortical activity. They studied EEG coherence in patients with suspected AD. Alpha coherence was decreased significantly in 6 patients. Significant delta coherence increase was found in a few patients between frontal and posterior regions. The group with AD demonstrated a significant decrease of alpha-band coherence in the temporo-parietooccipital areas. This was expressed to a greater extent in patients with more severe cognitive impairment. They theorized that these abnormalities could reflect 2 different pathophysiological changes: (1) the alpha coherence decrease could be related to alterations in corticocortical connections, whereas (2) the delta coherence increase suggests lack of influence of subcortical cholinergic structures on cortical electrical activity. Strik et al studied EEG microstates in AD. The microstates of the resting EEG of patients presenting with mild or moderately severe dementia of the Alzheimer type demonstrated a significant anteriorization of the microstate fields, and the duration of sustained microstates was reduced. These differences were more important than the diffuse slowing. The measurements of microstates may be useful in the early diagnosis of AD.[6 ]Muller et al conducted a study comparing SPECT and QEEG. They concluded that QEEG may be as useful as SPECT brain scanning in staging the disease; however, the correlation with clinical status was weak. [7 ] Akrofi et al used an automated coherence-based pattern recognition system utilizing multiple discriminant analysis (MDA) and kmeans clustering coherence features from EEG obtained from 56 subjects. Through statistical analysis, they were able to distinguish the patients with AD from the patients with mild cognitive impairment (MCI) and age-matched controls. This may indicate that patients with AD may have a greater number of damaged cortical neurons than patients with MCI and that MCI may be an intermediate step in the development of AD. [8 ] Siennicki-Lantz et al studied the relation of cerebral white matter lesions to AD.[9 ]Cerebral blood flow (CBF) in white matter correlated with systolic blood pressure and multichannel EEG in senile dementia of the Alzheimer type. The presence and functional significance of white matter lesions in the aging brain or in dementia and their relation to blood pressure is an unsettled issue. White matter lesions occur in both cerebrovascular disease and AD. Probably, the white matter lesions in hypertensive patients are not related to but simply are coexistent with the AD. Their influence on overall expression of the degree of dementia is unclear; intuitively, however, the lesions should be causing additional cognitive dysfunction. They observed significantly lower CBF in the white matter (WMCBF) in patients with AD than in controls. This was more obvious in the posterior cerebral region (ie, parieto-temporo-occipital area). QEEG from the posterior cerebral regions correlated with WMCBF. Systolic blood pressure was significantly lower in the AD group and was correlated positively with WMCBF in the posterior and anterior brain regions. Epileptiform activity may occur more frequently in patients with AD than in the general population; clinical tonic-clonic seizures can occur. Bilateral synchronous periodic epileptiform discharges (BiPEDs) (see the first image below), such as triphasic waves (TWs) (see the second image below), may be recorded in AD, usually in the late stages (for more information on TWs, see Triphasic Waveforms).
…medscape.com/article/1138235-print 5/40 .07/12/2010 EEG in Dementia and Encephalopathy: … Bilateral periodic epileptiform discharges (BiPEDs).
com/article/1138235-print 6/40 . QEEG and neuroimaging may be of great use in diagnosing and differentiating these dementia types.3%. and controls. They tried to differentiate patients with AD from the controls by QEEG and CBF measurements. epileptiform discharges or TWs are not predictive factors for seizures. While good correlation exists between severity of EEG abnormalities and cognitive impairment. Regional CBF and QEEG were correlated with one another. Significant correlations were found between Mini Mental State Examination (MMSE) scores and relative power of the 2. particularly hepatic encephalopathy and other degenerative diseases. QEEG and regional CBF sensitivity was 88% and specificity 89%. suggesting subcortical pathology. an impairment of the cholinergic system may have a relation to the EEG slowing that is characteristic of AD progression. Scheriter et al used clinical examinations. such as CJD. Hachinski scores and neuropsychological testing showed little difference between mixed dementia and AD. This study suggests that QEEG and regional CBF measurements used together are reasonably accurate in differentiating AD from healthy aging. [10 ] Used together. As would be expected.[11 ] ApoE sigma-4 allele is a risk factor for late-onset AD and is proposed to have an impact on cholinergic function in AD. patients with mixed dementias had more subcortical lesions with increased slow frequency power. while the correlation between MMSE scores and right regional CBF was less strong. maximum amplitude bilateral frontal.to 6-Hz and the 6.5to 12-Hz bands on either side and between MMSE scores and left regional CBF. neuropsychological testing and neuroimaging to see if distinctions could be made between patients with AD. and to confirm CJD when the dementia is rapidly progressive. Because the cholinergic system has an important role in modulating EEG. Rodriguez et al studied 42 patients with suspected AD and 18 healthy controls who were elderly.07/12/2010 EEG in Dementia and Encephalopathy: … Triphasic waves. The QEEG high-frequency power was normal in mixed dementia and decreased in AD. and regional CBF alone an accuracy of 75% in the whole group and of 71% in those with mild AD. To investigate the relationship between QEEG band powers and CBF. mixed dementia (vascular). with a total accuracy of 88. especially in the right hemisphere. EEG often can be useful in evaluating dementia in order to exclude a superimposed reversible metabolic etiology. likely reflecting the cortical pathology seen in AD. …medscape. These findings are not specific for AD because they most often are observed in metabolic disorders. QEEG. QEEG alone showed an accuracy of 77% in the whole group and of 69% in those with mild AD.
they tend to be juvenile cases. Genetic testing is far more useful. Posterior alpha rhythm is more preserved. The EEG in PSP may initially be normal but eventually shows increasing delta and theta activity as was the most common finding by Fowler and Harrison in 1986.[18 ]With disease progression. About 3% of the patients show epileptiform activity. 2 sigma-4. The EEG changes show gradual and progressive slowing over time. The EEG has not been proven to be of any predictive value in identifying future affected family members. Usually. midbrain atrophy and abnormal tau deposition. and histologically.13 ] The typical electrophysiological correlates of myoclonus in AD are similar to those of cortical reflex myoclonus. short REM latency. Pick disease Pick disease. These subgroups did not differ in clinical severity or duration of dementia. PET scan revealed severe cerebral glucose metabolic reductions in the frontal and temporal areas. About 30% of the patients have very-low-voltage EEGs with amplitudes below 10 microvolts. which is characteristic of dementia with Lewy bodies. [16 ]The study showed sleep fragmentation. …medscape. with a focal.07/12/2010 EEG in Dementia and Encephalopathy: … Lehtovirta et al studied the relation of apolipoprotein E (ApoE) to EEG changes. Frequency analysis may demonstrate a difference at a time when simple visual reading may not pick up a clear abnormality. and 0 sigma-4). The EEG is less abnormal than in AD. [12. Hyperventilation as a rule does not increase the background voltage as it usually does in healthy subjects. Temporal slow wave transients may be a useful diagnostic feature in DLB and may help to explain the transient disturbance of consciousness. The degree of such symptoms varies widely. and a severe reduction of slow wave sleep. Postmortem study showed severe neuronal loss. 1 sigma-4. is much less common than AD. V. Theta and delta are increased. Because EEG correlates poorly with the clinical symptoms. especially in the early stages. with relatively preserved NREM-REM sleep cycles. EEG findings in dementia with Lewy bodies and Alzheimer disease Briel et al found that 17 of the total 19 records from the patients with dementia with Lewy bodies (DLB) were abnormal. Progressive supranuclear palsy Progressive supranuclear palsy (PSP) causes decreased ocular motility. impaired postural reflexes. II. This new type of electrophysiological correlate of myoclonus may reflect activity of a subcortical generator. impressive EEG changes are not observed in this condition. spongiosis. [15 ]Stigsby demonstrated a decrease in anterior blood flow in patients with Pick disease. and gliosis most marked in cortical layers I.[14 ]Thirteen showed loss of alpha activity as the dominant rhythm. although the disease progression rate did not change. Huntington disease Huntington disease is a genetic condition characterized by movement disorder (primarily chorea). The major feature of Pick disease is a decline in judgment and insight with relative early preservation of memory. and psychotic features.and trans-hemispheric regional connectivity and of corticothalamic circuits. The QEEG of 31 patients with AD was recorded at the early stage of the disease and after a 3-year follow-up. In vivo. the EEG changes are not prominent frontally. Ingvar demonstrated these changes in 1977. contralateral negativity in the EEG preceding the myoclonic jerk. The amplitude also attenuates as the disease progresses. Gross et al found a decrease in background frequency of 6-7/s and delta activity over the temporal regions. Patients with AD were divided into several subgroups according to the ApoE sigma-4 allele (ie. rigidity. These findings suggest that the decreased cortical and subcortical connectivity may have been the main pathophysiological mechanism responsible for delta sleep reduction and the cognitive decline. Gemignani et al studied sleep in Pick disease with a longitudinal polysomnographic and 18-FDG-PET study. they found background slowing and frontal intermittent rhythmic delta activity (FIRDA) (see below) in this population. The electrophysiological correlate of polymyoclonus that can be seen in AD and other pathological states is a bifrontal negativity in the EEG that precedes the myoclonic jerk. neurometabolic and postmortem neuropathological data are consistent with and indicative of a severe dysfunction of intra. This slow wave transient activity correlated with a clinical history of loss of consciousness.[3 ]Because the anterior cholinergic system is relatively preserved in Pick disease. dementia. These differences in EEG may suggest differences in the degree of the cholinergic deficit in these subgroups. cognitive impairment. which is a frontotemporal dementia. and half had slow wave transient activity in the temporal lobe areas. The greater slowing of the EEG in DLB than in Alzheimer disease may be related to a greater loss of choline acetyltransferase found in DLB. They found that the delta often was rhythmic with frontal accentuation. Blood flow measurements correlate with thinking processes. The AD patients carrying the sigma-4 allele had more pronounced slow-wave activity than AD patients without the sigma-4 allele. The patients with Alzheimer disease were less likely to show transient slow waves and tended to have less marked slowing of dominant rhythm.com/article/1138235-print 7/40 .[17 ]Su and Goldstein et al found initial EEG patterns to be normal in 8 of 12 (67%) of patients with PSP. the degree of dementia is not severe. and VI. The age of onset is earlier than that of AD.
periodic leg movements and increased frequency of REM behavioral disorder.07/12/2010 EEG in Dementia and Encephalopathy: … Frontal intermittent rhythmic delta activity (FIRDA). All 5 patients with CBD had insomnia. EEGs revealed normal findings early in the disease and diffuse slowing that became more prominent with disease progression.[20 ] Parkinson disease The EEG is frequently normal. 4 had periodic limb movements and/or restless legs syndrome. The clinical neurophysiologic study findings were consistent with a cortical and subcortical degenerative process. Through the use of QEEG recordings in 6 patients with PSP as compared with controls. however. prolonged sleep latency. [22 ]Electromyograms (EMGs) and nerve conduction studies (NCSs) showed no abnormalities. Sleep may be markedly abnormal with frequent awakenings.[19 ]Frontal intermittent rhythmic delta activity was also observed but was not found to be specific to CBD. marked slowing is noted. Abnormalities of sleep architecture with REM sleep abnormalities were seen as well. Corticobasal degeneration Corticobasal degeneration (CBD) is a neurodegenerative disorder and tauopathy with progressive dementia and asymmetrical rigidity and limb apraxia. Roche et al evaluated 5 patients with CBD with none having REM behavioral disorder (as is often seen in many neurodegenerative disorders) or excessive daytime sleepiness.[21 ]The patients had PPND linked to chromosome 17q21-22. Serizawa et al compared patients with Parkinson disease (PD) with age-adjusted controls using QEEG and also found diffuse slowing in the patients with PD. reduced REM sleep. 11 EEGs of 9 patients were studied. Visual evoked potentials (VEPs) and sensory evoked potentials (SEPs) were normal. Wszolek et al studied patients with rapidly progressive familial parkinsonism and dementia with pallidopontonigral degeneration (PPND).com/article/1138235-print 8/40 . Tashiro et al found prominent focal slowing on EEG in the anterior and temporal head regions in early CBD in 8 of 10 patients studied. and 2 had sleep respiratory disorders. In advanced cases. Montplaisir et al found slowing over the frontal lobes in the waking state with neuropsychological testing confirming this frontal lobe dysfunction. …medscape.
Some background slowing may be observed. EEG can be useful in distinguishing the 2 conditions. The CT brain scan findings represented diffuse cerebral atrophy. such as bitemporal delta or bioccipital theta. one with occasional epileptic activity. focal theta or delta slowing may be observed. Kushner described patients with normal activity. They described a 72-year-old patient with von Recklinghausen disease exhibiting akinetic mutism within 6 months of the onset of dementia. Multi-infarct dementia No specific EEG pattern is associated with multi-infarct dementia. It can be made worse by attempts at precise or coordinated movement (ie.07/12/2010 EEG in Dementia and Encephalopathy: … With clinical deterioration. and one with asymmetric alpha depression. has been reported. The EEG records were pathological in most cases. On the other hand. [25 ] Circulatory Encephalopathy Atherosclerosis Plachinda et al studied the correlations of cognitive disorders and the EEGs of elderly patients with circulatory encephalopathy. After stereotactic surgery. Binswanger disease. Ninety-five patients (aged 60-74 y) with atherosclerotic encephalopathy but without stroke were included in the study. Autopsy findings revealed diffuse subcortical white matter disease and marked arteriosclerotic changes of the subcortical arterioles. patients with Korsakov syndrome have abnormal EEGs with slowing in the theta and delta frequencies. although action myoclonus may be limited to one limb in some cases of focal cerebral damage. Statistical analysis of the data demonstrated a correlation between psychological test results and EEG readings and computerized EEG data. The condition usually is associated with diffuse neuronal diseases. Theta and thetadelta mixture may be recorded bilaterally in the posterior head regions. Korsakov syndrome Obraztsova et al studied 32 patients (21 with reversible and 11 with chronic Korsakov syndrome of traumatic origin) and 20 healthy controls. Iznak et al used QEEG to reveal the specific features of and study amplitude-frequency parameters in patients with mild dementia of different origins compared with healthy elderly individuals.[26 ] In cerebrovascular disease. [23 ] Vascular Dementia Binswanger Disease Binswanger disease usually demonstrates slowing of background and a nonspecific pattern. therefore. The EEG demonstrated periodic synchronous discharges (PSDs) suggesting CJD. and the various forms of peripheral neuroepithelioma. Patients with AD were characterized by desynchronized EEG. They explored the possibilities of using EEG for evaluating intellectual-mnemonic disorders in elderly patients with cerebral atherosclerosis.com/article/1138235-print 9/40 . however. although it may be related to activity in the motor cortex relayed to the reticular formation preceding or coinciding with voluntary movement. progressive decline is seen in the mean parietal frequency and background rhythms. and the pathologic diagnosis confirmed Binswanger disease. and is believed to be caused by a vascular etiology or spreading depression. Nonepileptiform activity. can present with PSD and should be included in the differential diagnosis of dementia. with varying degrees of slow activity that was distributed symmetrically. Hereditary Encephalopathies Action myoclonus Action myoclonus consists of arrhythmic muscular jerking induced by voluntary movement. It is caused by hyperexcitability of the …medscape. [28 ]TGA caused by a seizure is uncommon. These changes are less prominent and do not show the progressive course observed in AD. Dzialek et al described a group of 15 patients with Binswanger subcortical atherosclerotic encephalopathy who showed a different EEG appearance.[27 ] Transient Global Amnesia A variety of records have been reported from normal to even epileptiform potentials in transient global amnesia (TGA). [24 ] The cortex was relatively spared. uremia. while 2 patients had intermittent rhythmic slowing. They found that EEG beta activity (13-20 Hz) in the frontobasal and brainstem locations had negative prognostic significance in Korsakov syndrome. Most typically. They found that alpha rhythm was suppressed in AD and vascular dementia and that alpha rhythm was slower and theta activity higher in AD. therefore. especially in advanced disease. The effective stimulus for action myoclonus is thought to be feedback from muscle afferents. intention myoclonus) and may be elicited by sensory stimuli. focal slowing is far more frequent than in nonvascular dementia. Kuroda et al reported some other patterns. such as posthypoxic encephalopathy.
Progressive background slowing. In the appropriate clinical setting. Autopsied cases have failed to reveal a clear pathology. and photosensitivity. and muscle fibers. Baltic myoclonus) is an autosomal recessive progressive myoclonic epilepsy syndrome. Unverricht-Lundborg disease Unverricht-Lundborg disease (ULD) (ie. epilepsy with ragged red fibers (MERRF) Isozumi et al described a 50-year-old woman with subacute dementia and myoclonus whose CT scan revealed brain atrophy and EEG revealed PSDs. the neurophysiologic features may aid the clinician in the diagnosis of this autosomal recessive inherited disorder. and focal occipital spikes are found on EEG. The flash VEP was usually abnormal and often asymmetrical. generalized spike and wave and polyspike and wave complexes. It may be associated with tonic-clonic seizures or dementia. the EEG is normal to slow. self-limited phenomenon reflects dysfunction of lethally damaged neurons. but is common in Finland. generalized epileptiform discharges. auditory. or both. Based on further investigations. and some patients with posthypoxic action myoclonus may improve with serotonin precursors. Zellweger syndrome This is characterized by diffuse slowing. consisting of progressive neuronal degeneration (ie. EEG studies have been carried out on 12 children with this condition. Myoclonus may be seen in degenerative disorders of the nervous system. Propofol often controls myoclonus but does not change the underlying condition. and prominent arrhythmic delta are present in temporo-occipital areas.to 22-Hz activity that is not reactive to environmental stimuli.[31 ]The onset is in early childhood and consists of intractable fits. Epileptic discharges usually do not occur in adrenoleukodystrophy. [30 ] Mitochondrial encephalopathy with lactic acidosis and stroke (MELAS) and myoclonus. cortical reflex myoclonus) or reticular formation (ie. pathological. and brain atrophy. the final diagnosis was mitochondrial encephalomyopathy. Clinical. hypsarrhythmic pattern. ULD is found sporadically worldwide. In general. reticular reflex myoclonus). The EEG abnormalities include BS-EEG. has been studied by Boyd et al. Poststereotactic surgery Patients developed EEG slowing of different degrees about 50% of the time. the EEG changes were described as background slowing. Myoclonus has been described in cases with Lafora inclusion bodies and cerebral storage diseases. multifocal epileptiform discharges. pyramidal. Neuronal ceroid lipofuscinosis …medscape. extrapyramidal. The myoclonus is severe and generalized seizures occur that are difficult to control. posterior columns and gracile and cuneate nuclei.com/article/1138235-print 10/40 . She initially was thought to be suffering from CJD but dramatically recovered over 5 months. Pantothenate kinase-associated neurodegeneration (PKAN) In PKAN. are seen in these patients.07/12/2010 EEG in Dementia and Encephalopathy: … sensorimotor cortex (ie. motor neurons of cranial nerves and anterior horns. formerly known as neurodegeneration with brain iron accumulation type I. spinocerebellar pathways. Alpers' disease This clinicopathological entity. 14. The EEGs were similar and demonstrated abnormal patterns with high-amplitude slow activity as well as lower amplitude polyspikes. [29 ]This transient. as well as system degenerations: cerebellodentatorubral. Theories include loss of inhibitory mechanisms involving serotonin and possibly GABA transmitters. progressive dementia. alpha-coma-EEG. Abnormal EEG patterns. Adrenoleukodystrophy Multifocal paroxysmal discharges. Generalized myoclonus Generalized myoclonus in comatose survivors after CPR implies a poor prognosis despite improvement of the critical care of patients. especially burst suppression EEG (BS-EEG) and alpha-comaEEG. Action myoclonus usually responds to sodium valproate or clonazepam. Infantile neuroaxonal dystrophy This condition is characterized by a high-voltage. and EEG findings indicate that these patients die from severe hypoxic-ischemic damage. Alpers disease) of childhood with liver disease. optic.
epilepsy may develop with minor motor seizures. and deceleration of head growth. autism. It appears to be sporadic in occurrence.07/12/2010 EEG in Dementia and Encephalopathy: … In the infantile form. Rolandic spikes may be elicited by noise. stereotypic "hand washing" movements. and epileptiform discharges. When affected girls are aged 2-4 years. diffuse spike and waves. These usually are present during wakefulness and disappear during sleep. A precise biochemical marker of this disorder has not been identified. the EEG is slow and early. …medscape.[32 ]The course is slowly progressive. in certain cases. apraxia. The EEG may demonstrate slowing. corresponding with the stage of dementia and cognitive decline. autistic behavior. sleep may attenuate the EEG abnormalities. and photomyoclonic and photoparoxysmal responses may be present. Epileptic activity is rare. Infectious Encephalopathies Creutzfeldt-Jakob disease The EEG shows a fairly typical repetitive pattern of BiPEDs (see first image below) such as TWs (see second image below) approximately 1-1. Tay-Sachs disease EEG is generally slow. and posterior spikes may be present. loss of purposeful use of the hands. seizures. slow-wave spikes. Generalized or multifocal spikes accompany the seizures. Gaucher disease In patients with type III disease. Photic response is excessive and evokes high-voltage spikes that are polyphasic. and paroxysmal delta slowing with spikes that may appear in sleep.com/article/1138235-print 11/40 . Al-Mateen et al reported 15 cases of Rett syndrome. Rett syndrome This is a progressive encephalopathy observed in girls. Rett syndrome consists of a progressive encephalopathy and psychomotor deterioration in young girls who have appeared clinically normal until age 6-18 months. When the child is at least 6 months old. Other signs include breathing dysfunction. posterior spikes and sharp waves. The epileptic activity may include multifocal spikes. it occurs only in girls and is characterized by early deterioration of higher brain function with dementia. According to McIntosh et al. however. The EEG abnormalities in the juvenile form are not as marked. Background flattening occurs to some degree. a variety of nonspecific patterns. [33 ]The incidence is similar to phenylketonuria and autism in females. Additional features may include an extrapyramidal disorder with dystonia and choreoathetosis. Metachromatic leukodystrophy Diffuse slowing progresses to high-voltage generalized delta activity. and loss of previously acquired skills. head growth decelerates in association with severe dementia.5 seconds apart. however. hypsarrhythmia may be observed. EEG abnormalities. and lactic acidemia. and growth retardation.
07/12/2010 EEG in Dementia and Encephalopathy: … Bilateral periodic epileptiform discharges (BiPEDs).com/article/1138235-print 12/40 . …medscape.
however. The cortices of the occipital lobes were damaged severely. Necropsy exhibited extensive gray and white matter lesions.07/12/2010 EEG in Dementia and Encephalopathy: … Triphasic waves. Aoki et al reported giant spikes with photic stimulation. PSDs seem to be the EEG hallmark of Creutzfeldt-Jakob disease. [34 ]These photic-stimulated giant spikes simultaneously suppressed PSDs. …medscape. optic nerve. The superior colliculus. and optic tracts were not affected. The Gennari line was spared.com/article/1138235-print 13/40 . Their findings indicate that the visual pathway may be involved in the generation of PSD in CJD (see below). Both lateral geniculate bodies and pregeniculate bodies were involved preferentially. maximum amplitude bilateral frontal. a number of atypical EEG presentations have been reported without these waveforms. The lesion of the lateral geniculate body appeared to be associated with the unusual EEG feature.
the Heidenhain 5 variant. They presented a pathophysiologic hypothesis on the development of PSWC based on the assumption that the specific periodicity of PSWC results from a still functionally active but greatly impaired subcortical-cortical circuit of neuronal excitability. periodic focal sharp waves were present at the left occipital region. as shown below. Lee et al reported a 73-year-old man presenting with visual symptoms. and rapidly progressive dementia. left more than right.com/article/1138235-print 14/40 .5 weeks). PSWC are usually absent in all other human prion diseases. myoclonus. The patient died within 5 months of presentation.07/12/2010 EEG in Dementia and Encephalopathy: … MRI axial diffusion weighted image: Cortical ribbon sign in CJD. laboratory data. like that shown below. 5 patients already had progressed to akinetic mutism characterized by loss of verbal contact and movement disorders (ie.[37 ] …medscape. EEG characteristics of CJD and its differential diagnosis were studied by Steinhoff et al. FIRDA-like EEG activities should be regarded as compatible with the diagnosis of CJD and should encourage further EEG studies for the demonstration of PSWC in a more advanced stage of CJD. and visual loss—ie. Diffusion-weighted MRI of the brain showed slightly increased signal intensity in the occipital parasagittal area. runs of frontal intermittent rhythmic delta activity (FIRDA). right hemianopia. The survival time is short after the onset of PSWC (average 8 weeks). They obtained a sensitivity of 67% and a specificity of 86%. Myoclonus was synchronous with generalized periodic epileptiform discharges on EEG. The EEG findings and the evolution of clinical signs were investigated by Hansen et al in 7 patients with CJD who underwent serial EEG recordings. In addition. Some patients with CJD presented with visual blurring. exaggerated startle reaction. At the onset (mean 8. They stressed the use of clinical signs. and EEG correlation and suggested that the clinical diagnosis of CJD should be reconsidered if repeated EEG recordings fail to reveal PSWC under technically adequate conditions. were found in all cases. They found some nonspecific EEG findings and also typical PSWC in the course of the disease.[35 ] These data help in the selection of EEG recording dates to detect PSWC in patients in whom CJD is suspected. diplopia. In earlier disease stages. The 14-3-3 protein was detected in the CSF. With the exception of one familial variant of CJD.7 weeks) of periodic slow-wave complexes (PSWC). or focal dyskinesia started in 5 patients). Occurrence of PSWC often related negatively to external stimuli and sedative medication. [36 ] Focal EEG abnormalities as described in the Heidenhain variant of CJD are uncommon. These were later replaced by PSWC in 6 patients. When akinetic mutism commenced (average 7.
This early periodic paroxysmal activity usually occurred at an intermediary stage. [38 ] Early periodic paroxysmal activity appeared within 12 weeks of the onset of the disease in 88% of the patients who underwent EEG recordings.[39 ] …medscape. segmental. thus ruling out a metabolic encephalopathy. and sensory or autonomic changes. when the patients demonstrated marked worsening of the clinical picture. and/or generalized myoclonic jerks were observed in 15%.07/12/2010 EEG in Dementia and Encephalopathy: … Generalized periodic epileptiform discharges (GPED). mental deterioration. and 100% of cases at prodromal. (2) periodic complexes with multiphasic configuration. Focal.com/article/1138235-print 15/40 . and asymmetrical myoclonic jerks. right-handed homosexual man who was admitted for progressive mental deterioration coexisting with permanent. respectively. EEG demonstrated frontocentral bursts of rhythmic triphasic 1. Evolution of clinical and EEG abnormalities were analyzed in all 20 (16 pathologically confirmed). Generalized or multifocal slowing may be observed. AIDS dementia EEG abnormalities usually precede brain atrophy on CT brain scan. and terminal stages. arrhythmic. middle-amplitude. and (3) periodic polyspiking discharges.to 2-Hz sharp waves similar to the characteristic periodic pattern of CJD. In 10 EEG recordings from 7 patients examined in the early clinical stage. Burst-suppression activity was observed frequently in the terminal stage in decorticate patients. Thomas et al described a 40-year-old HIV-positive. intermediary.5. About one half of patients who have normal neurologic findings on physical examination exhibit abnormal EEGs. Abnormal "pacing" by slowly repeated flashes was found in 4 patients presenting with visual hallucinations or cortical blindness. 53%. Different kinds of periodic paroxysmal activity were observed: (1) biphasic or triphasic periodic complexes. Illness duration was less than 4 months in 65% and greater than 17 months in 10%. segmental. no periodic discharges were present. asynchronous. Subacute spongiform encephalopathy Aguglia et al described 20 patients with subacute spongiform encephalopathy and periodic paroxysmal activities in the EEG. Biological investigations were negative. The early clinical stage was characterized by gradual gait disturbances. Computerized EEG is abnormal in most cases.
This movement disorder should be considered a rhythmic variant of cortical myoclonus.com/article/1138235-print 16/40 . Diehl et al followed 117 HIV patients with electroencephalography. [44 ] Chronic rubella encephalitis This condition is characterized by myoclonus. This unusual electroclinical presentation of the AIDS dementia complex underlines the fact that this condition presents a diagnostic challenge. Viral encephalitis Viral encephalitis frequently causes EEG abnormalities. ataxia. Serial EEGs on 117 HIV patients without any clinical signs of secondary neuromanifestations were studied in order to document electroencephalographic changes in the course of HIV infection. Intermittent rhythmic delta activity (IRDA) has been described. herpes encephalitis. mental deterioration. more polymorphic delta activity is observed. particularly in individuals in whom HIV infection has not been diagnosed previously. The results of this study indicated progressive CNS dysfunction with worsening of the immunostatus. Significant slowing of background activity occurred in the course of the disease. which produced absolute EEG normalization. Sinha et al described various electrophysiological abnormalities in HIV encephalopathy.[40 ]Electromyograph (EMG) recordings of the forearm muscles correlated with frontocentral electroencephalograph (EEG) rhythmic activity. see second image below). nonrhythmic temporal slowing. with diffuse slowing on EEG. In herpes simplex encephalitis (HSE) (see first image below). MRI axial FLAIR with gadolinium. temporal intermittent rhythmic delta slowing (TIRDA. left temporal. …medscape.07/12/2010 EEG in Dementia and Encephalopathy: … Dramatic neurological improvement occurred shortly after initiation of intravenous and then oral zidovudine. Canafoglia et al described a case of a HIV-seropositive patient with ataxia and upper limb rhythmic myoclonus. a periodic pattern may develop as the disease evolves. and frontotemporal slowing are characteristic. Periodic activity with spikes and slow-wave spikes may occur. and chorea.[42 ] Ferrari et al describe 2 patients with HIV type 1 infection who presented new-onset epilepsia partialis continua (EPC) as an early manifestation of progressive multifocal leukoencephalopathy (PML). HIV infection may have caused a dysfunction in the central nervous system pathways similar to that occurring in genetically determined conditions characterized by cortical myoclonus. Clinical signs of HIV-associated encephalopathy presented in 18 patients at the first examination and 23 at reexamination. If the cortical gray matter involvement is predominant. a rhythmic pattern (IRDA) is more common. [43 ]PML represents an increasingly recognized cause of newonset seizures in both seropositive and seronegative patients. [41 ] Polich et al found greater frontal delta power in HIV cases compared with controls. while with subcortical involvement.
[45 ] In a retrospective review of EEG in HSE. Al Shekhlee et al found periodic lateralized epileptiform discharges (PLEDs) (see image below) and/or focal temporal slowing present in 90% of the PCR-positive group (PCR testing for the herpes virus from spinal fluid being the most sensitive and specific test for the diagnosis of HSE) at symptom onset compared with 30% of the PCR-negative group.07/12/2010 EEG in Dementia and Encephalopathy: … Left temporal intermittent rhythmic delta (TIRDA).com/article/1138235-print 17/40 . Hsieh et al found abnormal EEG findings and abnormal neuroimaging in three fifths of children (n=26) with HSE aged 1-6 years correlated with poorer outcomes. They found that the sensitivity of the EEG recording for these focal and epileptiform findings decreases after 48 hours. The MRI results were consistent with HSE in 86% of those with HSE-positive PCR results obtained 48 hours from symptom onset. They found the EEG to be of important diagnostic use when obtained within the first 24-48 hours of HSE symptom onset. [46 ] …medscape.
The boy had a 3-year history of decreased vision.[47 ] Subacute sclerosing panencephalitis SSPE is a progressive. the background activity becomes suppressed. The EEG may provide an important clue regarding SSPE and demonstrates bilaterally synchronous. The EEG strongly suggested the diagnosis. One of the 9 patients had HIV co-infection. the patient demonstrated visual agnosia and early dementia. St Louis encephalitis Wasay et al studied electroencephalograms and magnetic resonance imaging (MRIs) of patients. The MRI findings in 2 of the 9 patients showed edema. Of the 9 patients who were examined with electroencephalography. The typical EEG findings and the presence of measles antibodies in the CSF confirmed the diagnosis of SSPE. particularly of the occipital lobes. SSPE had largely disappeared from the United States because of nearly …medscape. associated with a focal pigmentary retinopathy. On assessment. resulting in a burst-suppression pattern. although T-2 prolongation can be detected by MRI symmetrically in the cerebral white matter or multifocally in the subcortical white matter or cortex. should raise the possibility of SSPE. The longest interval (till date) between the visual symptoms and onset of neurological signs of SSPE was reported by the author. all 9 had seizures or other abnormalities. [48 ] SSPE should be considered in young patients who have persisting cognitive dysfunction that is not proportional to the severity of the initial trauma. MRI scan demonstrated symmetrical demyelination of the white matter. Serial EEGs usually capture PLED activity but in the later stages of the disease course. neurodegenerative disorder caused by defective measles virus replication in the brain as a consequence of measles immunization. Koppel et al reported on the relation of SSPE and HIV. Neuroimaging studies demonstrate nonspecific abnormalities or diffuse atrophy.com/article/1138235-print 18/40 . As SSPE progresses. even if neurological symptoms are absent initially. A focal pigmentary retinopathy. especially with macular involvement. and 1 had nonconvulsive status epilepticus.07/12/2010 EEG in Dementia and Encephalopathy: … Periodic lateralized epileptiform discharges. Repeated CT scans of the head were normal. highamplitude spike or slow-wave bursts that often correlate with clinical myoclonus. the EEG may revert to normal. Flaherty et al described a 17-year-old boy with SSPE discovered when he presented with confusion after a mild head injury.
with a course similar to that of the discharges observed in CJD.com/article/1138235-print 19/40 . EEG was characteristic of SSPE. periodicity. In 7-10 seconds. Brain biopsy and high measles antibody titers in the CSF confirmed the diagnosis of SSPE. [50 ] Fernandez-Torre et al described the clinical and electroencephalographic features of a comatose patient with severe anoxic encephalopathy who experienced acute reflex myoclonus precipitated by passive eye opening/closure and painful stimulation. high-voltage delta activity. PSDs were present for as long as 5 months. irreversible brain damage results in 4-8 minutes. …medscape. The first was HIV positive and presented with seizures and encephalopathy at the age of 21 months. MRI findings of the brain were nonspecific. Postanoxic EEGs may exhibit a variety of abnormal patterns: triphasic activity. but her mother had AIDS. Takahashi et al reported a 47-year-old man admitted to the hospital for depression. however. slow waves appear. Anoxic encephalopathy. This is followed by rhythmic. alpha coma pattern. As a rule. and burst suppression patterns with epileptiform discharges (Media file 10) nearly always carry a poor prognosis.[49 ] Metabolic Encephalopathies Metabolic Disorders Anoxic encephalopathy Hypoxia causes diffuse slowing in the EEG. Two children with SSPE were described. The wave pattern. she was not infected with HIV. repetitive complexes. and duration of appearance of PSDs were similar to those of PSDs seen in CJD.07/12/2010 EEG in Dementia and Encephalopathy: … universal measles vaccination. and bilateral PLEDs. The mechanism of occurrence is considered to be similar to that of PSDs in CJD. In some cases. subsequently. attenuation and EEG flattening occurs. burst-suppression patterns. Burst suppression pattern with bursts of spike and wave and polyspike wave discharges with voltage suppression. it has re-emerged in children infected with HIV. The acute and prolonged anoxia of cardiac arrest exhibits no changes initially. The second developed myoclonus and dementia at 4 years of age. The PSDs were prolonged gradually. showing high-voltage PSWCs and background slowing. establishing the completeness and duration of anoxia is difficult. who suddenly developed cardiopulmonary arrest of unknown etiology and entered a chronic vegetative state as a result of anoxic encephalopathy. Certain patterns carry a poor outcome: flat EEG.
and sensory stimulation-induced. [51 ] Comatose intensive care patients Young et al investigated the usefulness of continuous EEG monitoring. the diagnosis should be based on EEG evaluation and various types of stimulation. If prolonged coma ensues. were shown by Juvarra. and TWs may be recorded. in patients with long-term diabetes. bone destruction. and hypervitaminosis D. central. EEG changes appear when serum calcium level is approximately 13 mg/dL. In most cases of hypoglycemia. Addison disease Nonspecific slowing and diffuse theta and delta may be seen in a disorganized manner. polyspikes. the EEG changes persist and may become permanent. polydipsia.[53 ] Hypocalcemia. parathormone releasing tumors. epileptic activity may be observed with clinical seizure. Hypoglycemia The EEG resembles changes described with hypoxia. The pituitary adenoma is thought to be a major factor for FIRDA in this case. nonspecific slowing is observed in hyponatremic encephalopathy. muscle spasm and. Shortly after the anoxic insult. Cushing disease EEG changes are uncommon.to 7-Hz rhythm. They described acute and follow-up VEP and MRI findings of a patient with hyperglycemia-related visual SE of occipital origin.07/12/2010 EEG in Dementia and Encephalopathy: … Acute stimulus-sensitive postanoxic myoclonus is an underdiagnosed epileptic condition. The study suggests that CEEG monitoring may be more valuable for detection of seizures in patients with acute structural brain lesions (ASBLs) than in patients with metabolic encephalopathies. high-voltage. burst of high-voltage rhythmic delta. FIRDA may be associated with a small pituitary adenoma less than 10 mm in size. Muscle weakness.com/article/1138235-print 20/40 . When serum calcium is normalized. Photic driving may be prominent. slowing and intermittent rhythmic delta activity is seen. the EEG is usually mildly to moderately diffusely disorganized and slow. A variety of other patterns have been described: TWs. Hypercalcemia is associated with renal failure. Complicating factors included diffuse encephalopathy and use of antipsychotic drugs. the EEG usually improves but not immediately. Epileptic activity is very rare. sharp waves.[54 ]As soon as normalization of calcium serum level was achieved. however. high-voltage delta activity. EEG findings include theta and polymorphic delta slowing. rarely. Endocrine Conditions Adrenal disease EEG pattern is nonspecific. polyuria. Kameda et al reported a case of FIRDA in the EEG of a patient with pituitary adenoma. hyperventilation response is exaggerated and FIRDA may be observed. tetany. Twenty percent of patients recorded seizures. a generalized disorganization of record occurs. hypercalcemia Paresthesias. [52 ] Hyponatremic encephalopathy Usually. anorexia. nausea. The size of the pituitary adenoma that was proposed to be associated with FIRDA in the EEG recording was not noted. Occipital seizures and hemianopsia can be caused by hyperglycemia and may be accompanied by special MRI and VEP findings. Wang et al described hyperglycemia with occipital seizures. 5. rapid clinical and EEG improvement ensued. and paroxysmal activity. FIRDA remained in the EEG after these factors diminished. Pheochromocytoma No particular EEG pattern has been noted. A hypercalcemic condition can be observed in association with hyperthyroidism. among which diffuse monomorphic delta rhythms were remarkable. Hyperglycemia Similar slowing is the rule.[55 ] …medscape. Confusional state and EEG alterations. These should include passive eye opening/closure and painful stimuli. even in cases of clinical seizure. and coma may develop. and major depression. neoplasms. hyponatremic encephalopathy. seizures may occur in hypocalcemia.
This element has been demonstrated in plants and aquatic animals in nature. and under different clinical conditions in humans. Severe encephalopathy with confusion. and brain-stem auditory evoked response (BAER) in 7 children with glutaric aciduria type I (GA1). fatal convulsions in infants. [56 ] Three of the 7 patients showed abnormal EEG findings. The EEG may become abnormal months before the full-blown dementia develops. visual evoked potential (VEP). Subtle neurocognitive and psychomotor effects and EEG abnormalities have been reported at plasma aluminum levels as low as 50 mcg/L.[57 ]Aluminum toxicity is a major problem in agriculture. proportional and corresponding to the clinical alertness of the patient. [59 ] …medscape. One patient showed high amplitude bursts of beta in the occipital regions with left predominance while on clonazepam and baclofen. Malnutrition results in EEG slowing. Aluminum also is associated with dialysis encephalopathy.[30 ] Hypothyroidism Low-voltage theta is the rule with reduced photic driving response. The underlying metabolic problem has been suggested to be insufficient GABA synthesis.07/12/2010 Glutaric aciduria type I EEG in Dementia and Encephalopathy: … Neurophysiologic abnormalities are frequently seen in organic acidemias. the EEG abnormalities usually are diffuse slowing. although TWs may occur. Hyperthyroidism This has a nonspecific pattern. highvoltage spike and slow-wave complexes and paroxysmal bursts with a frequency of 2-4 Hz have been observed. Subcortical dysfunction may be present with FIRDA. Polymorphic frontally dominant delta often is observed. Yalnizoglu et al studied electroencephalogram (EEG). which often is accompanied by osteomalacia and anemia. affecting perhaps as much as 40% of arable soil in the world. Infants and patients with impaired renal function could be particularly susceptible to aluminum accumulation and toxicity. has been reported to cause subacute leukoencephalopathy. seizures and epiletiform discharges can be seen. EEG showed nonconvulsive status epilepticus (NCSE). including slowing and FIRDA. The background slowing usually correlates with severity of mental status impairment. developing several weeks or months after administration of carmofur. Cefepime Status epilepticus and encephalopathy have been reported with use of cephalosporins in patients with renal failure. Two patients showed asymmetry with intermittent occipital delta slowing in one hemisphere. In dialysis dementia. and at times. Aluminum accumulation occurs in the tissues of workers with long-term occupational exposure to aluminum dusts or fumes. Evidence exists to suggest that aluminum may be the causative agent in the development of dementia in patients with chronic renal failure who are on dialysis (ie.com/article/1138235-print 21/40 . Thiamine deficiency causes diffuse slowing in Wernicke encephalopathy. Symptoms were usually reversible but occasionally resulted in death. Toxic Agents Aluminum toxicity Flaten et al reported a wide range of toxic effects of aluminum. [58 ]Carmofur must be discontinued immediately if any psychomotor symptoms develop. delirium. This finding probably indicates underlying cerebral dysfunction and is not a specific feature. in experimental animals by several routes of exposure. Carmofur Carmofur. dialysis dementia). CT scan of the brains of severely intoxicated patients showed marked hypodensity of the entire cerebral white matter. Depending on the severity of the thyroid disfunction. Symptoms increased gradually even after stopping the drug. In fresh waters acidified by acid rain. Aluminum is a very potent neurotoxin. or coma developed. Kuzuhara described 3 individuals who developed subacute leukoencephalopathy after carmofur (l-hexylcarbamoyl-5-fluorouracil) administration. Maganti et al reported the case of a 79-year-old patient with normal renal function who developed subtle mental status changes during cefepime therapy for urinary tract infection. an antineoplastic derivative of 5-fluorouracil. The EEG demonstrated marked slowing. Initial symptoms were unsteady gait and dementia. Such effects also have been reported in certain patient groups without renal failure. Nutritional Deficiency Syndromes Pyridoxine deficiency causes severe. When seizure develops. aluminum toxicity has led to fish extinction. Such exposure may cause neurological effects.
valproate-induced hyperammonemic encephalopathy (VHE) is VPA treatment that results in elevated serum ammonium levels. Adams et al studied patients after liver transplantation. All of these patients had continuous high amplitude and generalized 2-4 Hz delta activity with intermingled spikes seen with episodes of unresponsiveness. See eMedicine article Lead Encephalopathy. The patient again was found to be in nonconvulsive status epilepticus with 3-4 Hz diffuse spike and wave discharges. Lambreva et al report a 60-year-old woman suffering from schizoaffective disorder who temporarily received 3 neuroleptics. coma. and an absence of triphasic waves on EEG. and nonconvulsive status epilepticus due to lithium toxicity and overdose is well documented. a patient presented in nonconvulsive status epilepticus with a normal serum lithium level that resolved with benzodiazepine administration and withdrawal of the lithium. The lithium was stopped. [64 ] Manganese encephalopathy Excess manganese (Mn) can cause several neurotoxic effects.[60. hyperammonemia. vomiting. She developed neurotoxic encephalopathy with symptoms of a malignant neuroleptic syndrome. The patient developed epileptic status. increased seizure activity.[67 ]Vinton et al reported TGB-induced nonconvulsive status epilepticus in 3 patients with focal lesional epilepsies—1 with initiation of the medication and 2 with recent dose escalation. If VHE is suspected. together with lithium. seizures. epileptic activity may be observed. These findings and other clinical symptoms usually resolve after VPA is withdrawn. Two months later. Herrero Hernandez et al described an epileptic syndrome due to manganese intoxication in a 3-year-old boy. Symptoms from acute poisoning may range from lethargy. Seizures were described in 13 (25%) patients. With this specific encephalopathic syndrome those on the above therapy may display excessive sleepiness or somnolence.[63 ]In a recent report by Bellesi et al.07/12/2010 Lead EEG in Dementia and Encephalopathy: … The heavy metal lead is usually absorbed into the body by ingestion and/or inhalation. Tiagabine Tiagabine hydrochloride (TGB) (an antiepileptic medication) is a selective gamma-aminobutyric acid (GABA) reuptake inhibitor that is used as an add-on therapy for partial seizures. They recommend frequent electroencephalographic controls for early detection of neurotoxicity. Lithium Encephalopathy. [68 ] Valproate and topiramate encephalopathy Panda et al reported 2 children with encephalopathy and slowing of EEG background activity. Generalized slowing in the theta and delta frequencies. topiramate-valproate induced hyperammonemic encephalopathy to describe the clinical features of patients on concomitant topiramate and valproate therapy. such as orthnithine carbamoyltransferase deficiency. and death to cognitive impairment. After dose reduction or withdrawal of the TGB and administration of IV clonazepam. cognitive slowing. the lithium was restarted with therapeutic levels attained. EEG and clinical signs normalized. never to be readministered. Chelating treatment promptly succeeded in reverting epileptic symptoms. serum ammonium levels should be evaluated and the existence of a possible urea cycle enzyme deficiency. confusional states. lethargy. [66 ]Kellinghaus et al reported 3 cases of recent increase in TGB doses causing nonconvulsive status epilepticus with the EEG of one of the patients demonstrating rhythmic delta waves.8% vs TGB alone 2. Seventeen (33%) of 52 patients who underwent 56 consecutive orthotopic liver transplants had serious postoperative neurological complications. In 3 patients. of these. should be considered. frontal intermittent delta activity (FIRDA). and triphasic waves can be found on EEG. drowsiness. The electroencephalogram (EEG) showed progressive encephalopathy.[65 ] Neuroleptic encephalopathy Treatment of psychiatric patients often necessitates overlapping neuroleptic medication. [70 ] Cheung et al proposed a novel term.7%). which promptly reverted to normal along with clinical improvement following withdrawal of valproate (VPA). which leads to a decreased level of consciousness. delirium. ataxia and distal motor neuropathy with chronic exposure.com/article/1138235-print 22/40 . 50% had onset of seizures within the first week. The risk of nonconvulsive status epilepticus can be elevated by TGB (comedication 7.[69 ] According to Segura-Bruna et al. the seizures were associated with postoperative metabolic encephalopathy and fatal …medscape.[71 ] Liver Transplantation The EEG in hepatic encephalopathy may consist of slow waves and TWs. and increased seizure frequency.61 ]Stewart et al found lead to be linked to neurodegeneration with cumulative exposure leading to decreased brain volumes and white matter lesions. [62 ]Treatment includes chelation therapy and removing the source of the lead exposure from the patient's environment.
The condition is steroid responsive. and transient ischemic attacks. or even paradoxically increased by. psychosis. On neuropsychological examination. Two types of initial clinical presentation can be differentiated: (1) a vasculitic type with strokelike episodes and mild cognitive impairment and (2) a diffuse progressive type with dementia. The EEG was abnormal in 90% of cases. and mild akineto-rigid extrapyramidal signs in one case and by apathy. [73 ] Hashimoto Myoclonic Encephalopathy Ghika-Schmid et al reported 2 patients with subacute diffuse encephalopathy characterized by confusion.com/article/1138235-print 23/40 . it showed nonspecific changes. abnormal VEPs were recorded in 5 of 32 patients (16%). EEGs were mainly normal or showed only slight nonspecific changes. Hietaharju et al evaluated CNS and psychiatric involvement in 32 patients. positive wave followed by a smaller negative deflection. and partial complex seizures in the other. memory deficit.[76 ]Most electroencephalographers now agree that TWs are a relatively nonspecific pattern observed in a number of metabolic conditions.[75 ]Encephalopathy typically affects patients when they are euthyroid and in an appropriate clinical situation. were initially described by Foley et al in hepatic encephalopathy. In addition. Severe CNS or psychiatric symptoms were present in 5 patients (16%). In a bipolar montage. and cerebral infarction could have contributed to the occurrence of seizures. seizures. scleroderma). toxic. psychotic episodes. and paraneoplastic causes need to be considered. Cyclosporin was thought to be causing the seizures in some of these patients. Since clinical features of Hashimoto encephalopathy are nonspecific. In others. steroid treatment for graft rejection. or altered consciousness. They later were described in other metabolic states and brain tumors. anticonvulsant treatment. This is expressed less in referential montages. grand mal seizures. myoclonic encephalopathy. who were not responsive to anticonvulsant medication but exhibited rapid neurological improvement following steroid treatment. Hashimoto thyroiditis with high titers of antithyroglobulin antibodies was diagnosed in both patients. TWs usually comprise a high-voltage.07/12/2010 EEG in Dementia and Encephalopathy: … progressive neurological deterioration. Triphasic Waveforms Triphasic waves (TWs). like those shown below. …medscape. Atrophy with temporal predominance was observed on MRI. and anoxia. A strong female predominance existed in this study. including encephalopathy. Kothbauer-Margreiter et al reported 6 patients with Hashimoto thyroiditis and associated encephalopathy and compared with 14 well-documented cases identified in the literature. predominant frontotemporal dysfunction was noted. A fronto-occipital (anteroposterior) phase lag varies from 25-140 ms. antithyroid autoantibodies are the main indicators of the encephalopathy. neoplastic. These observations support the idea that this potentially treatable dementia and movement disorder should be classified as a separate clinical entity. vascular. they usually are bilaterally synchronous and maximal frontally. These types may overlap. metabolic. suggesting optic neuropathy. anxiety disorder. 18 of the 20 patients were women. which was unresponsive to. other etiologies such as infectious.[74 ] EEG activity was remarkable for its rhythmic delta activity. [72 ] Scleroderma CNS involvement and psychiatric manifestations can occur in systemic sclerosis (ie. particularly over the long-term course in untreated patients. electrolyte disturbances. degenerative dementias.
the other had mild dementia associated with idiopathic calcifications of the basal ganglia and healthy auditory brainstem responses and subcortical and cortical SEPs. though they often were confused. TWs in a psychiatric population described by Blatt and Brenner carried a different prognosis. TWs have not been reported in children. usually severe. [77 ] EEG features analyzed included frequency of background rhythms.com/article/1138235-print 24/40 . One patient had coma associated with cerebellar hematoma. in 4. TWs were maximal posteriorly in 47 patients and anteriorly in 6 patients and were diffuse in 9 patients. thalamic gliomas . a history of seizures in 8. the TWs were maximal anteriorly. Aguglia et al concluded that TWs may result from focal brainstem/diencephalic lesions or from diffuse subcortical or multifocal encephalopathies in the absence of concomitant metabolic …medscape. Periodicity was prominent in 4 patients. distribution of the TWs. Generally.2 +1-1. Neurologic examination revealed no asterixis in either patient.7 [SD] Hz). in 2. However. [78 ] The literature on nonmetabolic causes of TWs also was reviewed. the cause was uncertain. Neuroimaging studies demonstrated prominent posterior abnormalities in only 1 individual. periodicity. and epileptiform abnormalities. and myoclonus in 4.326 EEGs performed from 1983-1992 in a psychiatric institute. patients with nonmetabolic diseases causing TWs presented with either disturbance of higher cerebral functions with no asterixis or sudden onset of coma. they occur primarily in elderly and severely demented patients. In a large retrospective study consisting of 15. Aguglia et al discussed nonmetabolic causes of TWs and described 2 patients with TWs on their EEGs in the absence of metabolic disturbances. Interictal epileptiform activity was present in 6 patients. the TW pattern carries a poor prognosis with a high mortality rate if it occurs in association with rapid neurological and clinical deterioration. multifocal cerebral lymphoma ). From the clinical point of view. cerebral carcinomatosis . Three patients suffered from diffuse subcortical or multifocal encephalopathies (Binswanger encephalopathy . pontine stroke ). All 62 patients were awake. Most (n=56) had dementia. although all were receiving lithium. 83 EEGs (62 patients—13 men and 49 women aged 59-90 years.07/12/2010 EEG in Dementia and Encephalopathy: … Triphasic waves. Seven patients had focal brainstem-diencephalic lesions (craniopharyngioma . Background rhythms were slow in all but 7 patients (mean 6. 15 also had delirium. Infrequent etiologies included neuroleptic malignant syndrome (n=1) and hepatic encephalopathy (n=1). maximum amplitude bilateral frontal. with a mean age of 74 years) had TWs. Six patients had no dementia. and the clinical and anatomic reports of 10 patients were analyzed. TWs are uncommon in psychiatric populations.
Etiology was linked more closely to level of consciousness at recording than any morphologic or distributional feature of the TWs themselves. a posterior-anterior delay or lag of the wave II peak occurred more commonly than did the better known anterior-posterior lag. different ways to calculate the data exist. routine digital recording of the clinical EEG by digital means does not add new information that was not present in the paper record. Although frequency bands are fairly well standardized. all 31 alert patients had nonmetabolic encephalopathies. seizures. TWs also were evaluated by Sundaram et al. In these patients. such as different montage displays and digital filtering. The original data must be evaluated before proceeding to further mathematical translation of this same data set. Some other methods. such as postconcussion syndrome. Lately.07/12/2010 EEG in Dementia and Encephalopathy: … abnormalities. alcoholism. schizophrenia. Prognosis for patients with either metabolic or nonmetabolic encephalopathies was unfavorable. Twenty-six (41%) of 63 consecutive patients with TWs had various types of metabolic encephalopathies. In this sense. a number of options become available for further analysis. while all 13 comatose patients had metabolic encephalopathies. brain map. usually senile dementia. These tests may be clinically useful only for patients well selected on the basis of their clinical presentation. Digital EEG As stated in the assessment report of the American Academy of Neurology and the American Clinical Neurophysiology Society. Forty percent of EEGs with sharp and slow-wave complexes (slow spike waves) had sporadically appearing TWs. while equally maximal waves I and II occurred next most commonly. A substantial risk of erroneous interpretations exists if any of the elements required is missing. most brain maps are not time locked to an event or brain state. Clinical use of any of the EEG brain mapping or other QEEG techniques by practitioners who are not physicians highly skilled and properly trained in …medscape. Spike recognition is an important enhancement and a great time saver but needs careful review by the interpreting physician. while 37 patients (59%) had nonmetabolic encephalopathies. digital EEG simply replaces and improves the paper record in ways similar to the way a word processor has improved letter writing by hand or even by a typewriter. attention disorders. therefore. coherence map). and storing a paper EEG record. learning disability. comparisons of frequency bands are difficult to accomplish across groups or disease states. no clear uniform recommendation has yet emerged. However. in addition. Normative values are being developed. equally maximal waves II and III were the most usual form. Thus. technologic developments have enabled the authors to record long-term monitoring on small storage devices. QEEG is not currently useful in civil or criminal cases. and sleep disorders much easier. The relative amplitudes of the 3 components differed from those of TWs in other conditions. EEG brain mapping visualizes some selected electrical event in the brain and maps its geographic distribution. Ideally. and their clinical correlates and morphology were assessed. Nonmetabolic causes of TW should be suspected in patients presenting with neurological disturbances not associated with asterixis.[79 ] The second. however. On the basis of available clinical and scientific evidence and expert opinions. depression. QEEG frequency analysis may be a useful adjunct to interpretation of the routine EEG. and operating room (OR) and ICU monitoring. QEEG is a derivative of regular EEG. Certain QEEG techniques are considered established as an addition to the digital EEG and include screening for possible epileptic spikes or seizures. TWs were not found to be specific for any single type of metabolic encephalopathy. In a number of conditions. EEG brain mapping and other advanced QEEG techniques should be used only by physicians highly skilled in clinical EEG and only as an adjunct to traditional EEG interpretation. TWs most often were expressed maximally anteriorly. simply enhance the visibility of the record. however. Continuous EEG monitoring by frequency trending helps to detect early intracranial processes in the OR or ICU (eg. Only 4 of 24 patients with metabolic encephalopathy and 1 of 35 patients with nonmetabolic encephalopathy were well at follow-up more than 2 years later. may bring into the forefront information that was already there in the paper record but is too tedious and time-consuming to calculate without use of a computer. Some processing methods. Among patients with metabolic encephalopathies. head injury. screening for possible epileptic seizures in high-risk patients in the ICU).com/article/1138235-print 25/40 . A clear definition for the clinical correlation of the brain maps is still needed. and drug abuse. long-term EEG monitoring or ambulatory recording. sufficiently well trained in mathematics and computing science should use these new technologies. such as calculating the mean band frequencies and different band-energy spectra. therefore. A thorough understanding and firm knowledge base in clinical EEG diagnosis may help prevent erroneous interpretations of digitally displayed mathematical constructs (eg. making the diagnosis of syncope. reviewing. only physicians properly trained in EEG and. the use of QEEG remains investigational. Once the paper recording is made. digital EEG is an established substitute for recording. No difference in quantity or mode of appearance existed between the metabolic and nonmetabolic groups when matched for consciousness level. Lags occurred with both metabolic and nonmetabolic conditions but were more common with the former. positive component (wave II) most often had the highest voltage. Attempts have been made to standardize some aspects of brain mapping.
as detailed in this article. on the other hand. they may not make the record more specific but merely easier to understand. In EEG practice. clear correlations and specific answers are desired. Personal perspective EEG often is compared with MRI. MRI is good at telling us where the lesion is. In such cases. Besides EEG. EEG has a definite role in evaluating changes in mental states. While interpreting MRI images. Computer analysis on the other hand may offer features that. although with computerization it may be improved. Clinical utility of EEG needs to be appreciated in a different way than some other diagnostic procedures. when this comparison is made. EEG study should be requested if clear clinical indications are present or if the clinician has a reasonable presumption that it may give clinically relevant information. EEG frequently is ordered to evaluate patients with different degrees of mental and behavioral changes and encephalopathy or coma. hence. Usually. The newer EEG techniques offer a number of conveniences and also enhance communication between the electroencephalographer and other clinical specialists. Nevertheless. the study may differentiate between a generalized and a focal abnormality. flat EEG and the appropriate clinical presentation may raise the suspicion of Huntington disease. It should help the referring source in diagnosis and treatment. and a number of clinical conditions can disturb the normal electrical field of the brain. EEG often is abnormal in subdural hematoma. since a primarily anatomical test is being compared with a functional one. the EEG may help in predicting the neurological prognosis. or to determine the extent of the abnormality for prognostic purposes (ie. EEG measures electrical field variations. a large number of conditions cause the EEG to appear abnormal.com/article/1138235-print 26/40 . therefore. the EEG does not give direct unequivocal information on the cause of the patient's condition. it usually refers to clinical MRI and not functional MRI studies. the clinician has to rely to a large extent on the clinical history and the neurologic examination findings to make a clinically meaningful conclusion. Conditions can be identified with EEG that as a rule cannot be seen on the MRI. this goal cannot always be achieved. A limited number of abnormalities that can be recognized in widely varied disease states exist. While the EEG is nonspecific. a normal EEG with preserved alpha might help establish the diagnosis of Pick disease. The EEG. nonspecific abnormalities are present that do not give definite information about the cause of the underlying process but do provide information on its location and severity. Simple state or electrolyte changes may alter the appearance and time variation of the brain-generated electrical fields. the correct question may be whether the EEG is normal or abnormal. In medicine. the EEG is almost always abnormal. and CJD. are difficult or time-consuming to extract and display. if the abnormality is generalized. while the EEG is pretty good at separating normal and abnormal primarily cortical function. When the patient has clinically symptomatic encephalopathy or moderate dementia. In cases of clinical dementia. therefore. The purpose of MRI is to provide precise localization of a lesion. the EEG helps resolve anxiety and supports a more correct ethical decision. This is promising and hopefully will soon become clinically useful and available. This comparison is puzzling. EEGs serve as a "proof" to families that indeed the brain function is disturbed so greatly that recovery is doubtful. the use of these studies is not exclusive but complementary. unless epileptic seizures are a consideration. But knowing exactly what these lesions represent is difficult on the basis of mere appearance. however. This may guide the clinician to further appropriate imaging studies. or renal encephalopathy. the EEG can be used to confirm clinical observation or suspicion. based on the modality and the underlying principle of measurement. while a slowed and shifted alpha frequency is seen in AD and PSP. In most instances. normal pressure hydrocephalus (NPH). primarily those of the cortex. Concluding Remarks The EEG is regarded as a fairly nonspecific measure of clinical states. although present in the regular record. On the other hand. It can confirm or refute nonconvulsive status epilepticus. usually one that has passed a certain stage of evolution. Topological usefulness of EEG is limited. the MRI scan is very sensitive in showing various lesions in the brain. Computer analysis of the EEG may help reveal subtle changes in AD. EEG is an important diagnostic tool in dementias in which specific morphological lesions are not apparent on imaging studies. On the other hand. the EEG can be used to characterize and monitor the disease process. however. therefore. attempting to predict outcome of the clinical condition). in most cases it is abnormal in altered mental states.07/12/2010 EEG in Dementia and Encephalopathy: … clinical EEG interpretation or without reviewing the original record should be unacceptable. The EEG may be used for the following: To exclude nonconvulsive status epilepticus …medscape. an abnormal EEG is a sensitive measure of brain function. This information is expected to alter the clinical decision-making process. Another role is to help the patient or family to understand the ongoing disease process. EEG changes are usually proportional to the degree of metabolic. With coma. the clinician relies to a large extent on other relevant clinical information. captures the changing electrical characteristics of a functioning brain. Sometimes. Low-voltage. The next step is to decide how an abnormal EEG would help the clinical diagnosis. hepatic.
To answer these questions. the cause of coma). or reasonably suspected. on the basis of clinical history and laboratory chemistry. nonspecificity is often not the question in general medical practice because most of the referrals in general neurology are individuals in whom the cause is pretty well clear.com/article/1138235-print 27/40 . SSPE To help a psychiatrist with the multitude of complex disorders masking as potential epilepsy or encephalopathy (eg. if any. CJD. However. lithium intoxication may present with BiPEDs) To identify focal or lateralized changes that suggest a structural cause to the encephalopathy The truth often is stated that EEG is nonspecific and cannot diagnose etiology or localization well (eg. metabolic encephalopathies) To attempt to record disease-specific patterns in the proper clinical setting. The question from the clinician is whether the brain is involved and the extent of brain damage. presently no clinical tool is more useful than the EEG. Multimedia …medscape. such as progressive myoclonic epilepsies.07/12/2010 EEG in Dementia and Encephalopathy: … To identify focal interictal epileptiform activity to confirm clinical suspicion that seizures may contribute to the condition in question To attempt to record functional disturbance in individuals whose brain MRI is "normal" but brain dysfunction is evident clinically (eg.
com/article/1138235-print 28/40 .07/12/2010 EEG in Dementia and Encephalopathy: … Media file 1: EEG in dementia. …medscape.
com/article/1138235-print 29/40 . …medscape.07/12/2010 EEG in Dementia and Encephalopathy: … Media file 2: Bilateral periodic epileptiform discharges (BiPEDs).
com/article/1138235-print 30/40 . maximum amplitude bilateral frontal.07/12/2010 EEG in Dementia and Encephalopathy: … Media file 3: Triphasic waves. …medscape.
07/12/2010 EEG in Dementia and Encephalopathy: … Media file 4: Frontal intermittent rhythmic delta activity (FIRDA). Media file 5: MRI axial diffusion weighted image: Cortical ribbon sign in CJD.com/article/1138235-print 31/40 . …medscape.
Media file 7: MRI axial FLAIR with gadolinium. left temporal.com/article/1138235-print 32/40 .07/12/2010 EEG in Dementia and Encephalopathy: … Media file 6: Generalized periodic epileptiform discharges (GPED). …medscape. herpes encephalitis.
com/article/1138235-print 33/40 . …medscape.07/12/2010 EEG in Dementia and Encephalopathy: … Media file 8: Left temporal intermittent rhythmic delta (TIRDA).
com/article/1138235-print 34/40 . …medscape.07/12/2010 EEG in Dementia and Encephalopathy: … Media file 9: Periodic lateralized epileptiform discharges.
Neuroreport. Alzheimer Dis Assoc Disord. [Medline]. Muscas GC. Reduced interhemispheric EEG coherence in Alzheimer disease: analysis during rest and photic stimulation. Dierks T. Helme RD. EEG slowing and cerebrospinal fluid tau levels in patients with cognitive decline. Decreased EEG microstate duration and anteriorisation of the brain electrical fields in mild and moderate dementia of the Alzheimer type. Siennicki-Lantz A. Chiaramonti R. 1998.com/article/1138235-print 35/40 . 9. O'Boyle MW.9(1):29-38. Akrofi K. [Medline]. 2. Widagdo MM. Age-related changes in qEEG during cognitive tasks.95(12):63-75. Jan 5 1998.51(5):537-47. 2008. [Medline]. Lilja B. Schiffer RB.07/12/2010 EEG in Dementia and Encephalopathy: … Media file 10: Anoxic encephalopathy. Muller TJ. Stevens A. Baker MC.2008:1092-5. Stigsby B.248(5):259-66. [Medline]. Kircher T. 6.9(1):157-60. Jul 1998. Sep 1998. 10. Clustering and modeling of EEG coherence features of Alzheimer's and mild cognitive impairment patients. Int J Neurosci. Jelic V.12(3):175-81. Rodriguez G. Thome J. Strik WK. Nobili F.247(5):259-63. Burst suppression pattern with bursts of spike and wave and polyspike wave discharges with voltage suppression. References 1. May 1981.75(3):183-91. Cognitive decline unlike normal aging is associated with alterations of EEG temporo-spatial characteristics. Nanbu Y. Pierson JM. Eur Arch Psychiatry Clin Neurosci. Rosen I. Psychiatry Res. Koshino Y. Eur Arch Psychiatry Clin Neurosci. Cerebral blood flow in white matter is correlated with systolic blood pressure and EEG in senile dementia of the Alzheimer type. 1997. [Medline]. Blomberg M. Quantitative electroencephalography and regional cerebral blood flow: discriminant …medscape. 8. [Medline]. 5. Dement Geriatr Cogn Disord. [Medline]. Oct 31 1997. Johannesson G. 4. 3. Ingvar DH. [Medline]. Chiaramonti R. 7. Rocca G. Conf Proc IEEE Eng Med Biol Soc. Electroencephalogr Clin Neurophysiol. Wada Y. [Medline]. A comparison of qEEG and HMPAO-SPECT in relation to the clinical severity of Alzheimer's disease. Jan-Feb 1998. Regional EEG analysis and regional cerebral blood flow in Alzheimer's and Pick's diseases.
107(3):213-22. 14.119(10):2255-9. Taniwaki T. Dec 1985. Derambure P. Comparison of quantitative EEGs between Parkinson disease and age-adjusted normal controls. 23. 28. Spectral analysis of EEG in Alzheimer's disease: relation to apolipoprotein E polymorphism. 3rd Ed. Neurol Neurochir Pol. 24. Sleep disturbances in progressive supranuclear palsy. Electroencephalogr Clin Neurophysiol. Ann Neurol. [Medline]. Ikeda A. Sep 1998. 31. [Medline]. Observations on comatose survivors of cardiopulmonary resuscitation with generalized myoclonus. Defebvre L.117(10):223642. Metabolic. 15. McKeith IG. 19. Hentschel F. Steg RE. Sattel H. Distribution of cerebral blood flow in the dominant hemisphere during motor ideation and motor performance.143(1):65-79. In: Ebersole JS. Occurrence of paroxysmal synchronous EEG discharges in subcortical arteriosclerotic encephalopathy (Binswanger's disease). [Medline].92(1):34-8.com/article/1138235-print 36/40 . Harden A. Feb 2005. Kuroda Y. [Medline]. Current Practice of Clinical Electroencpehalography. Kononen M. Neurosci Behav Physiol. Clinical neurophysiologic findings in patients with rapidly progressive familial parkinsonism and dementia with pallido-ponto-nigral degeneration. Sep-Oct 1998. [Correlations of cognition disorders and the EEG data in elderly patients with circulatory encephalopathy]. Oct 2004. Sharova EV. 1999. Hauser WA. Clin Neurophysiol. Thomke F. Klem GH.07/12/2010 EEG in Dementia and Encephalopathy: … analysis between Alzheimer's patients and healthy controls. EEG findings in dementia with Lewy bodies and Alzheimer's disease. Goldensohn ES. 18.37(4):261-4. Luders HO. 20. Intern Med. Morita A. Kononen M. Partanen J. Lehtovirta M. Barker WA. [Medline]. 12.2(3):230-7. [Medline]. 25. Okayama A. EEG findings in early-stage corticobasal degeneration and progressive supranuclear palsy: a retrospective study and literature review. 26. and hereditary encephalopathies. Dec 2008. Mar 1999. Spehlmann R. Kamei S. Oct 2008. Mizutani T. Sep 1977. [Medline]. 22. Gasser T. [Medline]. [Medline]. Characteristics of brain bioelectrical activity in post-traumatic Korsakov's syndrome. Oct 2006. Daniels JC.29(3):l83-6. [Medline]. Aug-Sep 2007. Serizawa K.18(6):684-91.25(6):361-6. Vestn Ross Ak ad Med Nauk . Belonog RP. Electroencephalogr Clin Neurophysiol. Rousson V. Gemignani A. Clin Neurophysiol. Jan-Feb 2000. Ingvar DH. Zh Nevropatol Psik hiatr Im S S Korsak ova. 11. Sep 1973. Kira J. Alzheimer disease versus mixed dementias: an EEG perspective. [Medline]. Electroencephalographic studies. Tashiro K. Zhigulskaia SE. Obraztsova ER. Hara M. et al. 21. Pietrini P. [The electroencephalographic image in Binswanger's subcortical arteriosclerotic encephalopathy].11(1):29-35. Boyd SG. Murrell JR. Marx JJ. [Medline]. [Medline]. Egger J. 29. Gavrilova SI. 16. Pedley TA. Transient global amnesia: a case-control study. Plachinda IuI. Kurohara K. Ann Neurol. A longitudinal quantitative EEG study of Alzheimer's disease: relation to apolipoprotein E polymorphism. Ogata K. [Medline]. Zaitsev OS. [Medline]. [Medline].9(5):27483.66(3):401-3. May-Jun 1989. 2005. Gross RA.5:14. Su PC. Destée A. Arch Ital Biol. Dzialek E. [Medline]. infectious. Ikeda A. Neurophysiol Clin. Sleep and vigilance in corticobasal degeneration: a descriptive study. Wszolek ZK. J Clin Neurophysiol. Lehtovirta M. Partanen J. [Medline]. Progressive supranuclear palsy. Jacquesson JM. [Medline]. Dement Geriatr Cogn Disord. J Neurol Neurosurg Psychiatry. Slow wave and rem sleep mechanisms are differently altered in hereditary pick disease associated with the TAU G389R mutation. Kushner MJ. Philipson L. Lippincott Williams & Wilkins. Monaca C.34(8):825-31. Lagerlund TD. Jul 1978. 2003:370-371.(1):11-6. Progressive neuronal degeneration of childhood with liver disease (Alpers' disease): …medscape. Iznak AF. Goto Y. Bogucki A. Arch Neurol.17(4):523-6.23(3):214-9. Noshchenko AG. 13. Roche S. [Quantitative EEG in early and differential diagnosis of mild dementia of different genesis]. [Medline]. 17. Yoshihashi H. 27. Schreiter Gasser U. Mar 1993. BMC Neurol.32(3):243-6. Neurobiol Aging. Szymanska R. Sauer O.45(1):16-25. Jul-Aug 1996. 1992. Dement Geriatr Cogn Disord. Briel RC. 30.
52(3):333-7. 44. Hsieh WB. [Medline]. Tan AK. Acute stimulus-sensitive postanoxic myoclonus: description of a case. Aug 1986. Chiu NC. [Medline].34(2):202-5.07/12/2010 EEG in Dementia and Encephalopathy: … characteristic neurophysiological features. O'Flaherty SJ. Oct 2000. Neurocrit Care. [Elecroencephalographic charactistics of Creutzfeldt-Jakob disease and its differential diagnosis]. Zschocke S. 41. Clin EEG Neurosci. Dec 11 1998.18(12):1533-8. A long-term study. Satishchandra P. Clin Electroencephalogr.13(1):17-9. May 2006. Sturenburg HJ. [Medline]. Takahashi M. epidemic. Diaz-Arrastia R. [Medline]. N Z Med J.24(4):166-72. 38. et al. Acta Neurol Scand. Riedemann C.40(1):34-8. Feb 2007. Gonzalez-Rato J.161(2):180-4.27(6):854-6. 48. Farnarier G. [Medline]. Franceschetti S. [Medline]. [Medline]. Herpes. Neurological deterioration following head injury: the eyes had it. 35. 51. 36. [Medline]. Loh NK. Jul 1987.36(3):199-201. Diehl B. [Medline]. Suarez JJ. Morbin M. Weston HJ. ERP. Sylvester E. Kropp S. 50. 34. [Medline]. Polich J. [Medline]. 47. Dec 2003. Young GB. Neuropediatrics. Arch Neurol. Mov Disord. 32. Kubota F. Nov 1998. Al-Mateen M. J Neurol Sci.17(2):75-80. and viral load. Panzica F. 46. Kocharian N. Fernandez-Torre JL. A commonly overlooked progressive encephalopathy in girls. Jibiki I. J Neuroimaging. Electroencephalogr Clin Neurophysiol. Ho CS. Int J Psychophysiol. Subacute spongiform encephalopathy with periodic paroxysmal activities: clinical evolution and serial EEG findings in 20 cases. [Medline].38(1):97-108. Oct 1993. [Medline]. Creutzfeldt-Jakob disease presenting with visual blurring. Kobayashi K. …medscape. Jun 1998. Huang FY. Sinha S. Dec 2003. Nishi Y. An autopsied case of Creutzfeldt-Jakob disease with the lateral geniculate body lesion showing antagonizing correlation between periodic synchronous discharges and photically induced giant evoked responses. 52. [Medline]. Outcome of herpes simplex encephalitis in children.2(1):5-10. [Medline]. Canafoglia L. Hu KC. Aug 1998. Thomas P. [Medline]. McIntosh RP.103(886):122-5. Clin Electroencephalogr. Poon TP. et al. Shields WD. Psychiatry Clin Neurosci. Nervous system involvement in asymptomatic HIV seropositive individuals: a cognitive and electrophysiological study. 49. Monaco S. Clinical changes and EEG patterns preceding the onset of periodic sharp wave complexes in Creutzfeldt-Jakob disease. Al-Shekhlee A. Continuous EEG monitoring in comatose intensive care patients: epileptiform activity in etiologically distinct groups. Mar 28 1990. [Medline]. [Medline]. Rett syndrome: case reports and review. J Paediatr Child Health. 45. [Medline]. Persistent synchronous periodic discharges caused by anoxic encephalopathy due to cardiopulmonary arrest. Apr 1998.6(2):122-5. Lee KE. Borg M. Neurol India. Tex. J Microbiol Immunol Infect. Steinhoff BJ.18(3):147-58. Routine electroencephalogram in follow-up of patients with HIV infections of different stages.51(4):466-9.97(2):99-106. Ilan A. Aguglia U. Nervenarzt.69(6):485-9. May 1986. Flaherty MP. Ferrari S. Doig GS. Suss RA. Re-evaluating the diagnostic methods in herpes simplex encephalitis. Reversible myoclonic encephalopathy revealing the AIDS-dementia complex. [Medline]. Apr 1996. Martinez-Martinez M.57(1):114-8. [Medline]. Tinuper P. HIV-associated PML presenting as epilepsia partialis continua. Ann Acad Med Singapore. Neuroelectric assessment of HIV: EEG. 43. Rett syndrome.66(8):357-65. Aoki T. Koppel BS. Poceta JS. Khandji A. Evers S. [Medline]. Simatos D. Am J Dis Child. 33. Feb 1998. Fortschr Neurol Psychiatr. 42.140(8):761-5. Subacute sclerosing panencephalitis and acquired immunodeficiency syndrome: role of electroencephalography and magnetic resonance imaging.com/article/1138235-print 37/40 .90(2):166-9. Philippart M. Wasay M. Rhythmic cortical myoclonus in a case of HIV-related encephalopathy. 40. Jul 2005. 37. diplopia and visual loss: Heidenhain's variant. Feb 1994. 2005. Jun 1998. 39. Hansen HC. Jan 2000. St Louis encephalitis: a review of 11 cases in a 1995 Dallas.
[Medline]. Ghika J.11(4):243-9. 54. 2009. 60. Nakayama H. Dec 2007. Kuzuhara S. 59. Sari N. Epilepsia. [Medline].medscape. Gunson B. Eur Neurol.1(8539):949-51. Acta Neurol Scand. 58.4(4):731-6.current status. Matkovic Z. Non-convulsive status epilepticus during lithium treatment at therapeutic doses. Jun 2002. Rodriguez-Campello A. Rishi D.20(2):157-60. Sep 2004. Puente V. Aug 1987. Lithium overdose causing non-convulsive status epilepticus--the importance of lithium levels and the electroencephalography in diagnosis. [Medline]. 63. et al. 69. Chen CC. Tiagabine-related non-convulsive status epilepticus in partial epilepsy: three case reports and a review of the literature. Holstege CP. Hashimoto's myoclonic encephalopathy: an underdiagnosed treatable condition?. [Medline]. [Medline]. Neurophysiologic features in glutaric aciduria type I. Jaaskelainen S. Schwartz BS. Radhakrishnan K. Stewart WF. Hong Kong Med J. Silvestrini M. Hypercalcemic encephalopathy in the course of hyperthyroidism. Fung CW.13(6):471-4. Dziewas R. Kameda K. Aug 2003. [Medline]. Subacute leucoencephalopathy induced by carmofur. Ghika-Schmid F. Neurotoxicology. Neurology. 62. Jan 2008. Manganese intoxication: the cause of an inexplicable epileptic syndrome in a 3 year old child. Wong V. Feb 2006. a 5-fluorouracil derivative. Kanemaru K. et al. O'Brien TJ. Itoh N. Huff JS. 1985. [Medline]. 72. Shen D. Acta Neurol Scand. Feb 2006. Segura-Bruna N. Kales SN. May 1993. J Toxicol Environ Health. 68. Mov …medscape. 57. Jul 2005. J Child Neurol. [Medline].87(5):3827. Bettoni L. Feb 2005.114(1):1-7.com/article/1174752-overview.26(6):444-6. [Medline]. 61. [Medline]. Saper RB. Provinciali L. AprJun 2005. Accessed November 11.48(6):527-41. Frontal intermittent rhythmic delta activity (FIRDA) in pituitary adenoma. 65. Ponsford S. J Clin Neurosci. Kilpatrick C. Bauer J. Jul 2006. Adams DH. Hietarinta M. 56. Roquer J. et al. [Medline].234(6):365-70.12(2):128-33. Lüdemann P. Cowley M. Bartolini M. Central nervous system involvement and psychiatric manifestations in systemic sclerosis (scleroderma): clinical and neurophysiological evaluation. Birchall JD. Herrero Hernandez E.47(2):153-8. Hyperglycemia with occipital seizures: images and visual evoked potentials. Passamonti L. Epilepsy Behav.46(7):1140-4. Ohkoshi N. et al. 64. Dassi P. Curr Drug Saf. [Medline].com/article/1138235-print 38/40 . 55. Valproate-induced hyperammonemic encephalopathy. Hietaharju A. Feb 2005. Neurological complications following liver transplantation. [Medline]. Karri SK. Two cases of valproate-induced hyperammonemic encephalopathy without hepatic failure.24(4-5):633-9. Cheung E. Flaten TP. Bellesi M. Davatzikos C. Alfrey AC. Tiagabine: efficacy and safety in partial seizures . Lead Encephalopathy.07/12/2010 EEG in Dementia and Encephalopathy: … 53. Aug 2008. Nonconvulsive status epilepticus due to cefepime in a patient with normal renal function. Lancet. Neurol Sci. Hsieh PF. Olivieri MF. Wang CP. Turanli G. eMedicine from WebMD. Available at http://emedicine. et al. 66. Kornberg AJ. Regli F. Lead encephalopathy due to traditional medicines. 71. 70. Jul 1995. Status and future concerns of clinical and environmental aluminum toxicology. [Medline]. Cooper-Mahkorn D. Past adult lead exposure is linked to neurodegeneration measured by brain MRI. Discalzi G.24(2):121-7. [Medline].26(3):173-9. Turk J Pediatr. Topiramate-valproate-induced hyperammonemic encephalopathy syndrome: case report.3(1):549. Neuropsychiatr Dis Treat. Jolin D. May 23 2006. Liu D. [Medline]. Juvarra G. [Medline]. 73. Seizure. Wu X. Tiagabine-induced generalised non convulsive status epilepticus in patients with lesional focal epilepsy. Yip KK. Rowden AK.66(10):1476-84. 74. Maganti R. Vinton A. Kellinghaus C. [Medline]. Yalnizoglu D. [Medline]. Panda S. [Medline]. 67. Yeung WT.8(1):312-4. Clin Electroencephalogr. J Assoc Physicians India. Apr 25 1987.52:746-8. J Neurol. Aug 30 1996.
Adv Neurol. triphasic waves …medscape. 89. 87. 79. PLEDs. Encephalopathy associated with Hashimoto thyroiditis: diagnosis and treatment. Adv Neurol. Kothbauer-Margreiter I. electroencephalogram. Neurol Sci. Keywords electroencephalography. 88. aging. 95.11(5):555-62. 99mTc-HMPAO regional cerebral blood flow and quantitative electroencephalography in Alzheimer's disease: a correlative study. Schwab RS. 78. 82. Trans Am Neurol Assoc. Locatelli T. Chung Hua Shen Ching Ching Shen Ko Tsa Chih. Blume WT.243(8):585-93. Ingvar DH. [Medline]. 76. Sep 1975. Cursi M.43:399405. 77. Significance of electroencephalographic changes in hepatic coma. Action myoclonus. Apr 1999. encephalopathy. 1986. Can J Neurol Sci. Neurology. [Medline]. Komor J. Triphasic waves: clinical correlates and morphology. 84.33(9):543-6. Jul 1990. Quadfasel FA. Using EEG in a consultative role.com/article/1138235-print 39/40 . [Medline]. Tatum WO 4th. 85. Ramsay Hunt syndrome. 81. [Medline]. cognitive decline. Isozumi K. Amantini A. A MELAS (mitochondrial myopathy. The EEG in organic disease. 63. [Medline]. Fukuuchi Y. 75. Parkinson disease. EEG coherence in Alzheimer''s disease. May 1987. Clin Electroencephalogr.106(3):229-37. [The cerebral ideogram]. England AC.41:242-248. Anoxic-ischemic alpha coma: prognostic significance of the incomplete variant. Encephale. Liberati D. Gambardella A. and other cerebellar myoclonic syndromes. Mar-Apr 1997. lactic acidosis. Nobili F. 1986. Aug 1996. Sep 1994. Foster MG. Peterson E.49(1):277-92. Comparison of EEG findings in Parkinson's disease. J Clin Neurophysiol. Mar 1998. [Medline]. J Neurol. 83. Xu CY. encephalitis. [Medline]. Sturzenegger M. Tanaka K.3(1):5-33. [An EEG evaluation in diagnosing subacute spongiform encephalopathy]. England AC.43:33-55. Alzheimer disease.21(3):120-5. Sep 1996. 91. and strokelike episodes) mtDNA mutation that induces subacute dementia which mimics Creutzfeldt-Jakob disease. quantitative EEG. Blatt I. QEEG. [Medline]. Feb 1989. Arch Neurol (Chicago). electroencephalographic. Triphasic waves in a psychiatric population: a retrospective study. Wilkins DE. Neurology. Sep 2003.24(6):397-400. Electroencephalogr Clin Neurophysiol. 90.50(5):1472-5. Rodriguez G.75:161-165. Oliveri RL.07/12/2010 EEG in Dementia and Encephalopathy: … Disord. 1948. Grippo A. 80. Bull Environ Contam Toxicol. Brenner RP.13(4):324-9. Watson CW. [Medline]. [Medline]. Aguglia U. J Nucl Med. quantitative EEG. May 1998. Cole AJ. Peterson E.9:65-72. Electroenceph Clin Neurophysiol. Dement Geriatr Cogn Disord. History of brain imaging in psychiatry. Adams RD. [Medline].7:275-288. Ingvar DH.10:186. [Medline]. [Medline]. 96.14(3):353-60.14(2):13640. Myoclonus in Alzheimer's disease and minipolymyoclonus. encephalopathy.8(2):66-72. 94. [Medline].23(3):295-306. 92. Foley JM. GPED. Jul 1997. Nuwer M. Fossi S. et al. Sundaram MB. Epileptic pseudodementia. CJD. Nonmetabolic causes of triphasic waves: a reappraisal. Rigid and akinetic forms of Huntington's chorea. Hallett M. Jul 1996. Assessment of digital EEG. and EEG brain mapping: report of the American Academy of Neurology and the American Clinical Neurophysiology Society. [Medline]. Semin Neurol. Neurology. Ross J. Intern Med. Schwab RS. Akinesia in Parkinson's disease.22(1):37-8. Proc R Soc Med. Drazkowski J. Lance JW. 1950. Bittenbender JB. [Medline]. 93. Copello F. The in vivo antifungal effects of benomyl on non-target soil fungi. cognitive impairment. [Medline]. 1958. 1962. et al. 86. [Medline]. 1977. Feb 2004.40(4):522-9. Hill D. 1959.
and American Medical Association Disclosure: UCB Pharma Honoraria Speaking. Departments of Neurology and Neurosurgery. MD is a member of the following medical societies: American Academy of Neurology. Sleepmed/DigiTrace Speaking. MD. eMedicine Disclosure: eMedicine Salary Employment Managing Editor Selim R Benbadis. and American Medical Association Disclosure: UCB Pharma Honoraria Speaking. consulting. Department of Neuroscience. New Jersey Neuroscience Institute. American Clinical Neurophysiology Society. Senior Pharmacy Editor. Pfizer Honoraria Speaking. consulting Chief Editor Selim R Benbadis. Bayfront Medical Center Florida Center for Neurology Erasmo A Passaro. consulting. PharmD.medscape. Comprehensive Epilepsy Program/Clinical Neurophysiology Lab. Glaxo Smith Kline Honoraria Speaking. UCB Honoraria Speaking and teaching. Professor. DO is a member of the following medical societies: American Academy of Neurology. Forest Honoraria Speaking and teaching Pharmacy Editor Francisco Talavera. Professor. and American Society of Neuroimaging Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching. American Academy of Sleep Medicine. Lundbeck Honoraria Speaking. Seton Hall University School of Graduate Medical Education. American Academy of Sleep Medicine. Tampa General Hospital Selim R Benbadis. New Jersey Neuroscience Institute-JFK Medical Center. UCB Pharma Honoraria Speaking and teaching. American Epilepsy Society. All Rights Reserved (http://w w w . American Medical Association. MD. American Clinical Neurophysiology Society.07/12/2010 EEG in Dementia and Encephalopathy: … Contributor Information and Disclosures Author Eli S Neiman. Pfizer Honoraria Speaking and teaching. Residency Program Director. Ortho McNeil Honoraria Speaking.com/article/1138235-print 40/40 . Comprehensive Epilepsy Center. Assistant Professor of Neurology. and Movement Disorders Society Disclosure: Nothing to disclose. Departments of Neurology and Neurosurgery. FAAN. JFK Medical Center. MD. DO. MD is a member of the following medical societies: American Academy of Neurology. American Academy of Sleep Medicine. consulting Acknow ledgm ents The authors and editors of eMedicine gratefully acknow ledge the contributions of previous author Leslie Huszar. JFK Hartwyck-Cedarbrook Philip A Hanna. Cyberonics. MD to the development and w riting of this article. American Clinical Neurophysiology Society. Ortho McNeil Honoraria Speaking. Director of Comprehensive Epilepsy Program. consulting. Neurology Director. consulting. Further Reading © 1994-2010 by Medscape. consulting. American Academy of Neurology. Huntington's Disease Unit. Pfizer Honoraria Speaking. American Epilepsy Society. Medical Editor Erasmo A Passaro. Lundbeck Honoraria Speaking. consulting. MD is a member of the following medical societies: Alpha Omega Alpha. University of South Florida School of Medicine. Inc Honoraria Speaking and teaching Coauthor(s) Philip A Hanna. Sleepmed/DigiTrace Speaking. consulting. consulting. Director. Director of Comprehensive Epilepsy Program. University of South Florida School of Medicine. NJ Eli S Neiman. consulting. and American Osteopathic Association Disclosure: UCB Pharma Honoraria Review panel membership. MD. consulting. American Epilepsy Society.com/public/copyright) …medscape. consulting. FAAN is a member of the following medical societies: American Academy of Neurology. consulting. MD. Associate Professor. Cyberonics Honoraria Speaking. Tampa General Hospital Selim R Benbadis. Edison. American Epilepsy Society. Glaxo Smith Kline Honoraria Speaking. Seton Hall University School of Graduate Medical Education. PhD. Cyberonics Honoraria Speaking.
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.