INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY Int J Geriatr Psychiatry 2005; 20: 1038–1045.
Published online in Wiley InterScience ( DOI: 10.1002/gps.1393 The utility of EEG in dementia: a clinical perspective Dimitrios Adamis1, Sunita Sahu2 and Adrian Treloar2,3 1Deptartment of Ageing and Health, Guy’s and St Thomas’ NHS Foundation Trust, London, UK2Old Age Psychiatry, Oxleas NHS Trust, Memorial Hospital, Shooter Hill, London, UK3Old Age Psychiatry, The Institute of Psychiatry, London, UK Despite being simple and cheap, the EEG is not often used in clinical practice.
Literature search using PUBMED and Medline.
Quantitative EEG can help to identify mild dementia and mild cognitive impairment and can increase diagnostic accuracy when used with other imaging techniques. EEG helps differentiate organic from functional brain disease and pre-dict response to cholinesterase inhibitors and is central in the diagnosis of Creutzfeldt Jacob disease. The accuracy of EEGmay be greater than that of CT or MRI scans alone.
Discussion Quantitative EEG may save on specialist interpretation time and enable more routine use of EEG in diagnosis and care. More widespread use of EEG’s is indicated. Agreement on the parameters that are best measured on qEEG is stillawaited. Copyright # 2005 John Wiley & Sons, Ltd.
key words — electroencephalography; dementia; psychiatric services; review by sleep, activity, medication and age. Delta waveshave frequencies below 4 Hz and may be regular or Few patients with dementia have biological brain tests irregular. Diffuse delta waves are normal in sleeping apart from CT and MRI scans. EEG provides informa- adults and children, but abnormal in awake adults.
tion about the physiological state of the brain both in They are the most common focal pathological wave- health and disease. Quantitative EEG (qEEG) uses form. Theta waves (4–7 Hz), are transiently present in computer software to provide topographic analysis 15% of the normal population. Alpha waves (8– of brain activity, allowing abnormalities to be 13 Hz) are normal in awake adults with closed eyes.
recorded on the outline of a head (Brain Electrical Prominent in occipital channels they are symmetrical Activity Mapping). Techniques such as Coherence and should disappear when the eyes are open. Beta analysis (Leocani and Comi, 1999) and Power Spectra waves (14 Hz and above) are normally present when analysis (Signorino et al., 1995) allow objective data the eyes are either open or closed. They are prominent to be provided without reliance upon subjective visual over the fronto-central regions and are increased by benzodiazepines, barbiturates, alcohol and anxiety.
(See Figure 1).
Activation procedures are used in epilepsy in particu- lar and include sleep deprivation, hyperventilation We searched Medline and Pubmed for recent publica- and photic stimulation. The EEG may be affected tions (1996–04) using key words Electroencephalo-graphy (EEG) and one of dementia, Alzheimer’s,Huntingdon’s, AIDS, HIV, Multi-Infarct, Creutz- *Correspondence to: Dr A. Treloar, Room 19 Memorial Hospital, feldt-Jacob, Fronto-Temporal, Lewy body and Parkin- Shooters Hill, London SE18 3RZ, UK. Tel: 020 8836 6407. Fax:020 8836 6381. E-mail: [email protected] son’s. We reviewed papers which suggested that EEG Copyright # 2005 John Wiley & Sons, Ltd.
nitively impaired individuals with elevated CSF tauprotein levels. Lehtovirta et al. (2000) found thatAD patients carrying the Apolipoprotein sigma4allele had more pronounced slow wave activity thanAD patients without the sigma4 allele. Examiningthe ApoE epsilon 4 allele, Jelic et al. (1997) foundthat ApoE epsilon4 allele does not influence EEGslowing but it was associated with a decrease in func-tional connectivity.
EEG as a predictor of dementia’s progression Berg et al. (1984) found that EEG did not predict pro-gression of dementias. Subsequently however, Helkalaet al. (1991) found that those with abnormal EEG inthe early stages of dementia had greater declines inpraxis, more extrapyramidal symptoms and a greater might be a useful diagnostic aid, or predict response risk for institutionalisation. Nobili et al. (1999) using to treatment. We then included relevant citations from qEEG in AD patients found that the loss of activities in daily living was predicted by delta power in eitherhemisphere, and incontinence predicted by alphapower on the right side. Claus et al. (1998a) also found slowing on qEEG to predict cognitive and functional The EEG identifies non-specific brain dysfunction in decline in AD. In another study (Claus et al., 1998b) Alzheimer’s disease. (Robinson et al., 1994). Can the found that mortality in patients with early AD was pre- EEG help to identify normal ageing form early dicted by a decrease in alpha and beta activity on spec- dementia or do changes only occur once the diagnosis tral EEG. Lopez et al. (1997) found that abnormal is clear? Anecdotal evidence suggests that the EEG is EEG at entry was associated with worse outcomes used more often as part of a diagnostic process in during follow up. Edwards-Lee et al. (2000) also younger patients, to differentiate functional illness found that EEG was worse in those with psychosis from organic early AD. Many studies (summarised in dementia. Jelic et al. (2000) studied a sample of in Table 1) have shown AD to relate to EEG. As well subjects with mild cognitive impairment who they fol- as distinguishing functional from organic disease lowed for 21 months using EEG. They found that the EEG can also distinguish very mild cognitive impair- important predictors for progression to AD were alpha ment from normal ageing. Indeed EEG may be more and theta relative power and mean frequency from left accurate than MRI or CT. Quantitative analysing temporal-occipital region which classified 85% of techniques, may increase the sensitivity of the EEG mild cognitive impaired subjects correctly. Therefore so that it can be used to differentiate normal aging EEG slowing early on in AD, does appear to predict from early dementia. But there is yet a lack of clarity about which are the best qEEG markers to identifymildly cognitively impaired subgroups that later pro- gress to clinically obvious AD. It may be that EEGand neuroimaging techniques used together (espe- The literature on ability of EEG to distinguish AD cially with rCBF) can increase diagnostic accuracy.
from MID is conflicting. Erkinjuntti et al. (1988)compared AD patients to MID patients and found that the degree of diffuse abnormalities and the mean fre-quency of background activity did not differ between EEG also has been used in research studies of Alzhei- the AD and MID groups. But Leuchter et al. (1987) mer’s disease in conjunction with biological markers reported that 92% of subjects with either AD or like Apolipoprotein E and tau protein. Jelic et al.
MID were accurately classified using discriminate (1998a) found CSF (Cerebrospinal fluid) tau protein analysis of both EEG frequency and coherence.
to be related to the EEG alpha/delta ratio. No such Further studies with EEG tried to resolve this pro- correlation was found in healthy controls or mild cog- blem. d’Onofrio et al. (1996) suggested that qEEG Copyright # 2005 John Wiley & Sons, Ltd.
Int J Geriatr Psychiatry 2005; 20: 1038–1045.
Studies of EEG use in diagnosing Alzheimer’s dementia Studies of moderate to severe dementia; Increased slow activity and decreased mean frequency correlate with cognitive impair- Weiner and Schshrer (1956), Coben et al.
Severity of EEG abnormalities and cognitive impairment correlated.
Correlation between cognitive deficit and both theta increase andconcomitant fast beta activity decrease.
Brenner et al. (1986, 1989), Adler et al.
Differentiation from depression with 69%–84% accuracy Increased global theta power decreased left temporal alphacoherence and decreased interhermispheric thetas coherence inAD patients compared with cognitively normal depressedcontrols. The left temporal alpha coherence and global thetapower allowed an identification of AD patients with a sensitivityof 87% and a specificity of 77%.
Pijnenburg et al. (2004), Prichep et al.
Synchronisation likelihood differentiates AD from subjective memory impairment. Beta synchronisation helps to distinguish AD from controls and Mild Cognitive Impairment.
Increase in theta power present in earlier stages of AD.
Reduced beta band synchronisation in early and mild AD.
Resting state alpha dipolarity (D(alpha) distinguishes early ADfrom normal controls.
Topography of beta and delta, delta activity, and amplitude ofdelta activity gave a sensitivity and specificity of over 90%discriminating AD patients from normal subjects.
Temporo-parietal coherence a discriminate variable togetherwith alpha and theta relative power between AD patients andcontrols giving a 77.8% sensitivity and 100% specificity.
Proposed the use of power ratios (ratios between fast and slow Visually assessed EEG, found a high specificity of 89.1% and a sensitivity of 44.6% to diagnose AD in a memory clinic.
Brenner et al. (1986), Dunkin et al.
Good correlations between EEG and psychometric tests.
(1995), Strijers et al. (1997), Rodriguez Eight-degree scale correlated with the severity of cognitive impairment 19 channel EEG, mild dementia (n ¼ 17) and Generalised frequency [È] highly correlated with MMSE scoresand performance IQ scores of the Japanese WAIS.
Early onset AD have a different pattern of spectral parameters qEEG was more accurate (81–84%) than MRI (72%) in AD patients diagnosed using the CAMDEX. Noted incompleteoverlap of the two groups suggesting that if used together,accuracy would be further enhanced.
Muller et al. (1997a), Pozzi et al. (1996) qEEG better correlated with clinical severity than SPECT.
Montplaisir et al. (1996), Claus et al.
AD patients with lower frontal perfusion were no different on qEEG from normal subjects but the usefulness of qEEG for the diagnosis of dementia is restricted to a subgroup of patient with aSPECT pattern of parietal blood hypoperfusion.
REM sleep on qEEG more useful than SPECT in mild tomoderate AD.
EEG related to CT scans to some degree.
qEEG alone had an accuracy of 77% for the whole group(normal vs AD) and of 69% in mild AD. When qEEG and rCBFwere used together, accuracy was 88.3%. The sensitivity of bothprocedures was 88% and specificity was 89%. rCBF and qEEGappear to be the best predictors of AD severity.
Copyright # 2005 John Wiley & Sons, Ltd.
Int J Geriatr Psychiatry 2005; 20: 1038–1045.
is a useful ancillary test to differentiate MID from EEG in In Lewy Body (LBD) and Parkinson’s AD. A more recent study by Moretti et al. (2004) also concluded that analysis of the alpha frequency and The abnormalities reported in Parkinson’s disease power can discriminate mild AD from Vascular dementia consist of non-specific diffuse changes such dementia and normal elderly subjects. Sato et al.
as slowing of background rhythms posteriorly and an (1996) found differences in EEG component waves increase in theta and delta activity (Brenner, 1993).
between normal and MID subjects. Coherence studies Wszolek et al. (1998) studied patients with rapidly have shown that long distance coherence is more progressive familial Parkinson’s and dementia with affected than local coherence in AD whereas the pallido-ponto-nigral degeneration. EEG revealed opposite occurs in MID. (Leuchter et al., 1992, Comi abnormal findings early in the disease and diffuse et al., 1998). Pucci et al. (1998) showed that EEG slowing became more prominent as the diseases pro- spectral parameters could discriminate between AD gressed. Fogelson et al. (2003) found EEG response and MID. Jeong et al. (2001) using nonlinear methods with rivastigmine treatment in PD patients with of analysing EEG, found differences between AD and dementia. The changes were characterised by an MID. Seal et al. (1998), using qEEG during odour increase in faster frequencies and they concluded that detection and during serial subtraction correctly clas- this may indicate increased arousal or improvements sified 95% and 91% of subjects with AD or MID, in the cognitive status of the patients as a consequence respectively. But using brain autopsy Muller et al.
(1997b) found few correlations between EEG and cer- Crystal et al. (1990) reported a slowing of the pos- ebrovascular pathology. So on balance, while EEG terior background rhythm and often a frontally domi- may might distinguish pure MID from pure AD this nant burst pattern in neuropathologically diagnosed can probably be done just as well clinically. Of LBD cases. They suggested that EEGs could help to course, most patients have mixed MID/AD.
differentiate AD from diffuse Lewy body disease.
Briel et al. (1999) reported a greater slowing of the EEG in LBD than in AD. However Londos et al.
(2003) using EEG and rCBF and Barber et al.
The EEG in Pick’s Disease is often associated with a (2000) using EEG suggested that these could not dis- normal EEG (Stigsby et al., 1981). EEG coherence is tinguish between AD and LBD. A small study by also no different from normal controls but delta and Calzetti et al. (2002) suggested that the FIRDA (Fron- theta powers were significantly increased in AD com- tal Intermittent Rhythmic Delta Activity) could dis- pared to frontal lobe dementia subjects. (Forstl et al., tinguish AD and LBD patients and could improve 1996). A study by Yener et al. (1996) found that using the diagnostic accuracy of LBD. Therefore the role five qEEG measurements they could reach an accu- of EEG in LBD and PRD is unclear. The EEG is only racy of 84.6% to distinguish between FTD and AD likely to predict response to treatment, if this was also and 100% from controls. The most informative qEEG useful for Alzheimer’s patients (see below).
variables for distinguishing FTD and AD were rela-tive power from the temporal region in beta-2 bandand from the parietal region in the theta, alpha andbeta-2 bands. A combination of qEEG and neuropsy- chological testing was the best predictor of FTDaccording to Lindau et al. (2003). Chan et al.
A significant increase of coherence in qEEG in (2004) reported no significant difference in EEG patients with AIDS, with or without cognitive impair- appearance between FTD patients and AD patients ment, has been reported particularly in long distance connections (Newton et al., 1994). Alpha rhythmchanges are the earliest non-specific signs of HIVbrain involvement. Elevation of alpha amplitude was associated with change in the mental state. Anti- The EEG is abnormal in HD with low voltage in about retroviral medication suppresses this alpha elevation 40% (Scott et al., 1972). Streletz et al. (1990) found supporting the usefulness of qEEG in monitoring increased theta and decreased alpha activity in patients the effect of the drugs on the CNS (Baldeweg and with HD. However the EEG does not predict which Gruzelier, 1997). Also the reduction of intrahemi- family members will eventually develop HD, and spheric alpha coherence correlates with the degree would never approach the accuracy of gene testing.
of cognitive impairment. (Fletcher et al., 1997).
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Int J Geriatr Psychiatry 2005; 20: 1038–1045.
The MACS study (Nuwer et al., 1992) has reported no difference in the incidence of EEG abnormalities in seropositive subjects when compared with serone- Cholinesterase inhibitors shift activity patterns of gative controls. Parisi et al. (1989) reported that EEG EEG towards normal (Agnoli et al., 1983). Jelic abnormality might be a predictor of CNS involve- et al. (1998b) studied the longitudinal changes of ment. Again, however, the diagnostic and severity qEEG during long term tacrine treatment of patients indices of HIV dementia are not those of EEG abnorm- with AD. They found slowing of fast EEG frequencies alities—rather, in HIV they are immunological and provided some evidence of early decline in treatment effectiveness. Four studies (Alhainen et al., 1991,Alhainen and Riekkinen, 1993, Knott et al., 2000,Almkvist et al., 2001) found that qEEG profiles after a single test dose of Tacrine, were good predictors ofresponse to Tacrine. Studies with Rivastigmine have In contrast Creutzfeldt-Jakob disease is associatedwith ‘Periodic sharp wave complexes’ (PSWCs), found similar predictive capacity of EEG. (Adler which are highly characteristic of CJD (Levy et al., and Brassen, 2001, Brassen and Adler, 2003, Adleret al 1986). Steinhoff et al. (1996) found a specificity of ., 2004). Alpha and Delta frequencies in qEEG 86% and sensitivity of 67% in a blind EEG analysis are also reduced by donepezil in AD (Reeves et al.
for PSWCs. PSWCs may exceptionally disappear in 2002; Balkan et al. 2003). In a longitudinal study of the terminal stages of the disease (Aguglia et al., mild to mopderate AD patients, Rodriguez et al.
1997). Periodic sharp waves are usually generalised, (2002) found that qEEG deterioration is reduced by but they can be focal or lateralised (Cambier et al., Donepezil. Kogan et al. (2001) examined the long- 2003). Although PSWCs have also been reported in term effect of donepezil on the qEEG of 12 AD cases of severe post-anoxic encephalopathy, herpes patients at different stages of their illness. Patients encephalitis, AIDS dementia, lithium toxic encepha- with mild AD showed reduced mean absolute theta lopathy, Binswanger’s disease and severe AD (Rosen, activity in frontal and temporo-parietal areas. Thosewith moderate/severe AD showed decreased mean 1996), these clinical situations can be distinguishedusing history or laboratory tests. Steinhoff et al.
absolute beta 1 activity particularly in the frontal (1998) presented a pathophysiological hypothesis on and occipital areas. A recent study by Onofrj et al.
the development of PSWCs based on the assumption (2003) showed that donepezil had a better effect in that the specific periodicity of PSWCs results from patients with fluctuating cognition than those without.
still functional but greatly impaired subcortico- They found that EEG could identify patients who cortical circuits. This specific pattern of neuronal fluctuate and therefore predict the response to the degeneration may very rarely arise in other diseases treatment. In Parkinson’s Related Dementia too, independent of their aetiology so that EEG patterns increased relative alpha activity has been seen with appear identical. They suggest the use of clinical rivastigmine treatment (Fogelson et al., 2003). These signs, laboratory data and EEG to reach a diagnosis studies (some of them were open label) suggest that of CJD. On the contrary, a clinical diagnosis of CJD EEG is altered as a result of therapy with Cholinester- should be re-evaluated if repeated EEG recording fail ase inhibitors, and might usefully predict response in to show PSWCs. Hansen et al. (1998) investigated EEG findings and the evolution of clinical signs. They concluded that PSWCs usually mark the terminalstage of CJD. In early stages FIRDA-like EEG activ- The EEG is a relatively simple and inexpensive non- ities (Frontal Intermittent Rhythmic Delta Activity) invasive diagnostic tool which has a high sensitivity should be regarded as compatible with the diagnosis for distinguishing organic brain disease from func- and further EEGs requested to demonstrate PSWCs tional. This in itself is an asset in so far as there is in advanced stages of CJD. Van Everbroeck et al.
often diagnostic uncertainty in mid to late life when (2004) using WHO diagnostic criteria observed EEGs new psychiatric diagnoses occur in previously well typical for CJD in 52% of the autopsies with ‘defined’ individuals. The identification of organic disease in CJD a rate that was less than other previously such circumstances could help to guide treatment.
reported. They found the PSWCs in 52% of the Better secondary prevention of further disability by CJD patients, in three of the AD patients, in one with encouraging treatment of lipid, sugar and lifestyle might result. Once an organic diagnosis is clearly Copyright # 2005 John Wiley & Sons, Ltd.
Int J Geriatr Psychiatry 2005; 20: 1038–1045.
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