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Dementia
and Geriatric Dement GcriatrCogn Disord 1997;8:1997;8:110-116
Cognitive Disorders
K e y w o rd s Abstract
EEG Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a
Dementia high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low
specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson
dementia, and in these conditions the degree of EEG abnormality is correlated with the dis
ease severity. Quantification of EEG makes these correlations more reliable and provides a
method for monitoring therapeutic effects. Dementias with predominantly frontal pathology
show much less EEG abnormality, and in these conditions the EEG is often normal despite
obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an
early stage of clinical evaluation, EEG may be useful in the discrimination of organic demen
tia from pseudodementia, because EEG is usually normal in depression, confusion, agitation
and other psychiatric conditions. In pscudodementia due to intoxication with sedatives the
EEG is usually dominated by diffuse p activity. At the stage of differential diagnosis of an
organic brain disorder, EEG cannot reliably discriminate between encephalopathies second
ary' to hydrocephalus, AIDS, cerebrovascular disease, B|i deficiency and primary' degenera
tive diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular
lesions, metabolic encephalopathies, i.c. of hepatic origin, Creutzfeldt-Jakob disease, herpes
encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorat
ing mental and neurological condition. Repeated EEG recordings over time would add signif
icantly to the diagnostic information. New techniques such as topographical brain mapping,
analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the com
bination of quantified EEG techniques with evoked potentials and event-related potentials
will presumably add to the sensitivity as well as the specificity of the electrophysiological
methods in the diagnosis of dementia.
Electroencephalogram -Basic N europhysiology frequencies in the 8-13 Hz (a) range and is generated by
several independent generators in the cerebral cortex and
The electroencephalogram (EEG) is a recording of cere thalamus [3], Slow waves between 0.5 and 4 Hz (8) prevail
bral electrical potentials by electrodes on the scalp. It is a during the deep stage of normal synchronized sleep but are
spatiotemporal average of synchronous postsynaptic po scarce in the normal waking condition. Both metabolic
tentials arising in radially oriented cortical pyramidal cells. and structural pathology can give rise to diffusely distrib
Synchronous neuronal activity arises by various mecha uted polymorphic 8 activity. Cholinergic deafferentation
nisms. Specific pacemakers exist in the thalamocortical may play a role in the production of cortical 8 activity [4-
neuronal circuitry' that produce rhythmic synchronous ac 6], Localized 8 activity is usually attributed to a lesion with
tivity. These are under the influence of afferents from the some destruction of cerebral tissue. The pathophysiologi
brain stem reticular formation, which stimulate individual cal mechanisms of slow waves in the 4- to 8-Hz range (0) is
neurones into independent asynchronous activity. These not well known. Often, 0 activity represents a slowing
effects are mediated by cholinergic and noradrenergic neu down of the a activity and in these cases represents the
ronal systems. Thus, synchrony is reduced by arousal and dominant background activity. There is a relationship
increases with reduced vigilance [1, 2], The rhythmic between the dominant or mean EEG frequency and the
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activity of the normal adult awake EEG is dominated by rate of cerebral blood flow and oxygen uptake in cortical
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background activity [14, 15]. In a few studies, attempts have been published on the subject of EEG and dementia.
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Tool in D em entia
particularly verified or probable dementia of Alzheimer [cf. also 53]. The heterogeneity of DAT was further illus
type (DAT), well over 500 during the last 10 years. trated with multichannel brain mapping applied to two
EEG. conventionally interpreted, shows a high per groups of DAT patients, one with predominant memory
centage of abnormalities in DAT [35-39]. Most of these deficit, and one group with progressive spatial impairment
studies also showed a correlation between the degree of [54, 55] with differences located to the parietal region.
EEG abnormality and the severity of dementia. Systema Mapping studies usually show a widespread increase of 0
tized blind interpretation of EEG [40] in 86 patients with and 8 activity, and a more localized decrease of a and [3
DAT showed abnormal findings in 87.2% at the initial activity [28,55-57], Breslau el al. [58] found marked asym
examination, and in 92% at follow-up. A normal EEG had metry' of8 activity over temporal lobes, in correspondence
a negative predictive value of 0.825 with respect to the with the PET findings ofFricdland ct al. [59],
diagnosis of DAT. i.e. a sensitivity not found with other Patients with Down’s syndrome developing early or
imaging techniques. A group of patients with probable ganic dementia similar to DAT show EEG abnormalities
DAT and depression was found to have abnormal EEG. similar to those described for DAT [60-62],
whereas patients with depression or depressive pseudode Two groups have independently found frequency anal
mentia had normal EEG or only mild abnormalities [41]. ysis of EEG during REM sleep onset superior to wake
This has recently been confirmed with quantified EEG EEG for the differentiation of mild DAT from normal
techniques [42-44]. controls [63-65] and from cognitively unimpaired seniors
A large number of studies have been reported, compar with major depressive disorder [44],
ing different quantitative EEG variables in patients with EEG mapping studies have revealed time segments of
DAT with other types of dementia and age-matched con spatially stationary map landscapes as characterized by
trol subjects. The criteria for the clinical diagnoses as well the locations of potential maxima and minima. The seg
as the degree of dementia vary to a large extent and are not ments of EEG activity were significantly fewer and the
always well defined. In only a fraction of the patients the segments lasted longer in DAT patients compared to con
diagnoses have been verified by post mortem histological trols [66]. The gross distribution of rhythmic EEG activity
examinations. In mild DAT. relative 0 power [45, 46] and of various frequencies can be estimated by FFT-dipolc
dominant occipital frequency [43] seem to provide the approximation. DAT patients showed a shift of a and 3
highest sensitivity, in the latter study with a correct classifi activity toward frontal brain regions and the degree of
cation rate of 77% in DAT versus control subjects. In the shift correlated with the degree of dementia [67],
study of Penttila et al. [46], using one single channel for On a semiquantitative level, early studies [68] found a
quantification, slowing of the occipital peak frequency and correlation between rCBF reduction in postcentral areas
distinct accentuation of relative 6 power only occurred in and an increase of EEG abnormality. On a quantitative
cases of advanced DAT. In a longitudinal study [47] over level the regional EEG frequency did not correlate with
2.5 years relative 8 and 0 power increased and a and (3 rCBF. although a significant correlation with white mat
power as well as mean frequency decreased in correlation ter blood flow was found [69]. A few studies have been
with the disease progress. Again relative 0 power most unable to demonstrate clear-cut correlation between EEG
effectively distinguished between four stages of dementia. and SPECT abnormalities [17, 70], Patients with DAT
Two groups of DAT patients, one with normal or slightly with relative intactness of parietal lobe function as mea
abnormal EEG. and one with abnormal EEG were followed sured by psychometric testing and FDG-PET showed
for 1 and 3 years [48-50]. Despite progression of the dis preservation of the EEG a background [71 ]. In a mapping
ease, the EEG of the first group deteriorated more slowly as study [72] anterior horn distance, lateral ventricle dis
compared with the second group, and showed less decline tance, Evan’s index and cortical density in CT correlated
of practice, naming and automatic speech functions, less with the degree of 8-0 increase and a-3 decrease in EEG.
extrapyramidal symptoms and less risk of institutionaliza
tion. Patients with the most marked slowing of the domi
nant occipital rhythm were found to have the lowest con Differentiation between D A T and
centrations of noradrenaline in the thalamus [51] and the Cerebrovascular Dementia
lowest levels of choline acctyltranferasc activity in frontal
cortex at the postmortem examination [52], These results Several studies have compared patients selected on clin
indicate a heterogeneity of DAT and that EEG at the onset ical grounds to suffer from DAT and multi-infarct demen
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of the disease might predict the rate of disease progression tia (MID), respectively. The results obtained seem to
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EEG can be repeated without the limitations inherent EEG in Creutzfeldt-Jakob Disease
with radioactive isotope techniques (rCBF. SPECT.
PET), and have been extensively used for testing of psy About 200 reports have been published since 1975
choactive drugs [pharmaco-EEG, 81]. In DAT. phvsostig- describing EEG in this rare (incidence about 0.4/million)
mine infusion produced significant improvement which disease. The characteristic feature is diffuse or focal slow
correlated with rCBF changes [82], It has also been uti ing developing into periodic sharp wave complexes
lized in trials with oral tetrahydroaminoacridine [83, 84], (PSWC). The PSWC pattern appears within 12 weeks of
The pretreatment EEG as well as drug effect on EEG dif disease in 88% of the cases, usually correlated with a
fered in clinical responders and nonresponders. Electro- marked worsening of the clinical picture [93-95], Focal or
physiologic brain mapping has also been found useful in asymmetric PSWC arc common at onset (about 50%)
trials in DAT patients with CDP-choline [85], and several with correspondence with focal clinical signs. A subgroup
nootropic drugs [72]. The effect on quantitative EEG of of patients (10%) had unusually long courses, and showed
single intravenous doses of scopolamine has been suggest PSWC in only 55%. The EEG pattern is not pathogno
ed as a test of the degree of cholinergic deficiency in Alz monic for Creutzfeldt-Jakob disease and has been re
heimer’s disease [86], ported in cases of severe postanoxic encephalopathy [96],
AIDS dementia complex [97], herpes encephalitis [98],
lithium toxic encephalopathy [99. 100], Binswanger’s dis
EEG in P ic k 's Disease and Frontal Lobe ease [101], and severe DAT [102].
Dem entias
EEG in patients with histologically verified frontotem EEG in Dementia of V arious Aetiologies
poral cortical atrophy were found to be normal or moder
ately abnormal despite prolonged dementia of increasing EEG changes are uncommon and mild in alcoholic
severity [37, 68]. Quantified EEG showed a moderate and dementia unless it is combined with hepatic encephalopa
diffuse increase of relative 9 activity in a group of fronto thy [103, 104], EEG is usually normal in neuro-psvcholog-
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temporal dementia patients, identified by their clinical ically unimpaired patients infected with / / / f ' [ 105], In
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Tool in D em entia
Fig. 1 . Practical use of EEG as a diagnostic tool in dementia.
AIDS and AIDS-related complex, the incidence and sever dialytic encephalopathy is characterized by synchronous
ity of abnormal EEG increases with the development of and symmetrical frontal intermittent rhythmic 8 waves
AIDS-related dementia with diffuse and/or focal slowing and frontocentral spike waves [ 108] (fig. I).
and in 10% focal epileptiform activity [106]. In normal
pressure hydrocephalus the EEG shows a diffuse slowing
A cknow ledgem ent
which is correlated with the CSF outflow resistance. The
EEG response to a CSF tap test was not significant and Supported by the Swedish Medical Research Council, grant No.
therefore of limited diagnostic value [ 107]. Progressive B95-14X-0008A-31B.
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