THE ELECTROENCEPHALOGRAM IN PSYCHIATRY · Electroencephalography and Clinical Neurophysiology.) (b) Percentage distribution of sedation thresholds in mg./kg. body weight for psychotic

POSTGRAD. MED. J. (I963), 39, 34

THE ELECTROENCEPHALOGRAMIN PSYCHIATRY

L. G. KILOH, B.Sc., M.D., M.R.C.P., D.P.M.Reader, Department of Psychological Medicine, University of Durham; Hon. Consultant, Royal Victoria Infirmary,

Newcastle upon Tyne, and Newcastle upon Tyne General Hospital*

AT present the interpretation of electroencephalo-grams is necessarily an empirical process. When-ever interpretation is attempted, a prediction ismade which is entirely a matter of probability. Itis rarely possible therefore to state with confidencethat a particular pattern is diagnostic of anyspecific clinical entity. Seldom is it advisable toclaim more than that the EEG findings support orfail to support the diagnosis suggested by theclinician. In many conditions-and this isparticularly true of psychiatric disorders-theincidence of abnormal records is relatively low andthe finding of a normal EEG does nothing toexclude the possibility of such an illness. Only ina few conditions, such as cerebral abscess orsubacute progressive encephalitis, is the incidenceof abnormality so high that the finding of a normalEEG virtually rules out its existence. The requestmade by so many clinicians to the electroen-cephalographer, to exclude a certain condition, ison the whole an unreasonable one.

Apart from the fact that normal EEG findingsare frequent in the presence of indisputabledisease, the repertoire of the EEG is very limited:so that specific patterns of abnormality are conse-quently rare. The same appearances are com--monly produced by a variety of conditions ofwidely differing atiology, and it is a dangerouspractice to attempt to correlate EEG abnormalitieswith specific pathologies. In psychiatry theposition is made even more difficult by our limitedknowledge of etiological factors and by lack ofagreement on such matters as classification.

Personality and its Disorders.There is general agreement from a number of

surveys that between io and 15% of the popula-tion at large have ' abnormal' EEGs-abnormal,that is, in a statistical sense. The abnormalityconsists of an excess of theta activity (4 c/s. up tobut excluding 8 c/s.) sometimes with delta com-ponents (less than 4 c/s.) often best seen in thetemporal areas. Such an EEG is usually describedas 'immature', but it must be emphasized that

* Present appointment: Professor of Psychiatry,University of New South Wales, Sydney, Australia.

this does not necessarily mean that the patient isimmature in any other way (Fig. i). It doeshappen that the more carefully subjects areselected -for stability, the smaller the incidence ofsuch abnormalities. Thus Williams (I94I) foundthat this pattern of EEG abnormality was presentin only 5% of flying personnel as compared withio% of other servicemen. The incidence ishigher (25%) in mixed groups of psychoneuroticsand highest of all (65 to 83%) in aggressivepsychopaths.

Hill (1952) found in a series of I94 non-epilepticpsychopaths that in addition to an excess ofbilateral theta activity, i4% of cases showed fociof 3 to 5 c/s. activity in the posterior temporalareas (Fig. 2). Although usually bilateral andsymmetrical, these were sometimes more promi-nent or limited to one side, commonly the right.Such slow activity, whether focal or not, is usuallyirtermixed with normal cortical rhythms, and isusually more responsive to eye opening and otherphysiological stimuli than is the not dissimilaractivity sometimes produced by certain patho-logical cerebral states.These so-called immature patterns occur nor-

mally in children (Fig. I), but once again when oneselects children with behaviour disorders, onecommonly finds that the EEG is relatively im-mature in 50 to 6o% of cases, containing slowactivity of a frequency or amplitude characteristicof a younger age group.

In patients experiencing nocturnal enuresis, theEEG investigations of Ditman and Blinn (1954-55)have shown that the patients fall into two groups,those who micturate in a state of deep sleep andthose whose EEGs show a waking pattern whenmicturition occurs. The former is usual inchildren, the latter in adolescents and adults.These findings suggest that the members of thelatter group are awake but in a state of dissociationwhen they micturate, for they remain unresponsiveto stimuli and unaware that they have done so.

PsychoneurosesIn patients suffering from anxiety states there

tends to be less alpha activity and an increase inthe amount of faster rhythms. Similar changes

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(a) (b) (c)FIG. i.-(a) Normal EEG. Male aged 36 years. Alpha rhythm at 8j c/s. (b) Immature EEG. Female aged 20 years.

8 c/s. alpha rhythm intermixed with irregular theta components. (c) Normal EEG. Boy aged io years. 8 c/s.alpha rhythm intermixed with irregular theta components.

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FIG. 2.-Aggressive psychopath. Male aged i8 years. Occasional focal delta waves in posterior temporal areas on abackground of irregular theta and alpha frequencies.

occur when anxiety is induced in normal subjectsand they appear to be related to preoccupationwith anxious thoughts, for a well-marked alpharhythm is a resting phenomenon and is easily lost-or blocked-by mental activity. A good alpharhythm can often be elicited in anxious patientsby sedation (Fig. 3). Apart from the higherincidence of immature patterns, no particular EEGfeatures occur in patients with hysteria orobsessional states.

In 1952 Gibbs and Gibbs described the occur-rence of runs of 14 and 6 c/s. positive spikes

during sleep in patients suffering from attackswhich they claimed to have a thalamic or hypo-thalamic origin. Other observers have noted ahigh incidence of headaches, neurotic symptoms,behaviour disorders and syncopal attacks inpatients showing this phenomenon (Refsum,Presthus, Skulstad and Ostensj6, I960), butothers have failed to confirm these findings (Walter,Colbert, Koegler, Palmer and Bond, I960). Theexistence of the I4 and 6 c/s. positive spikephenomenon must be accepted but its precisesignificance is still very much in doubt.

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POSTGRADUATE MEDICAL JOURNAL

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FIG. 3.-Anxiety state. Female aged 35 years. (a) Traces of alpha rhythm posteriorly with muscle artefact anteriorly.(b) Following sedation: mixed alpha frequencies posteriorly with low voltage beta runs anteriorly.

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FIG. 4.-(a) Sedation threshold. Normal subject. Ordinate: mean amplitude of frontal fast activity in ,uv. Abscissa:integrated amount of amylobarbitone sodium given intravenously in mg./kg. body weight. Arrow indicatesinflection point corresponding to point of slurred speech. (From Shagass, 1954). (By courtesy of the Editor,Electroencephalography and Clinical Neurophysiology.) (b) Percentage distribution of sedation thresholds inmg./kg. body weight for psychotic and neurotic depression groups. Mean sedation threshold for psychotics:2.23 mg./kg. Mean sedation threshold for neurotics: 3.99 mg./kg. (From Nymgaard, 1959.) (By courtesy of theEditor, Archives of General Psychiatry.)

Manic-depressive IllnessIn manic-depressive illness about 8o% of

patients have normal EEGs. Not surprisingly,records similar to those seen in patients withanxiety states occur frequently, containing littlealpha rhythm but an excess of fast activity. Thereis a tendency for the alpha frequency to be

relatively high in cases of mania and low in casesof depression.The sedation threshold test (Shagass, I954)

provides results which have great interest thoughthe practical value of the procedure is limited.When 0.5 mg./kg. body weight amylobarbitonesodium is given intravenously every 40 seconds,

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FIG. 5.-Catatonic schizophrenia. Male aged 36 years. Burst of theta activity with low amplitude spikes posteriorlyon a background of alpha rhythm at 9j c/s. and random theta activity.

the resulting clouding of consciousness and slur-ring of speech are accompanied by the appearanceof I5 to 30 c/s. activity best seen in the frontalareas. The amount of this fast activity may bemeasured by means of a frequency analyser. Whenthis is plotted against the quantity of amylo-barbitone sodium given, a curve is obtained show-ing an inflection point which approximates in timeto the onset of slurred speech (Fig. 4a). Thetotal amount of amylobarbitone sodium in mg./kg.body weight given up to this inflection point is anindex of the sedation threshold. It is unrelated tosex or age. Amongst neurotic patients the valueis correlated with manifest anxiety, and Shagassand Jones (1958) found that the mean value incontrols was 3.09 mg./kg., in hysterics 2.79 mg./kg.,in anxiety hysteria 3.9I mg./kg., in obsessivecompulsive states 4.42 mg./kg., in neurotic de-pression 4.78 mg./kg., and in anxiety states 5.27mg./kg. A striking difference was noted betweencases of neurotic and endogenous depression, themean level being 2.8I mg./kg. in the latter groupregardless of the amount of agitation present(Fig. 4b). Some authors, such as Nymgaard(I959) have confirmed these findings; others

(Ackner and Pampiglione, I959) have failed to doso.

SchizophreniaMany studies of the EEG in schizophrenia have

been reported, but because of differing diagnosticcriteria, many are not comparable. There seemsno doubt that in the majority of cases the EEG isnormal, and that when abnormalities do appear,they vary widely from case to case. Early reports of' choppy ' records (Davis, I939), that is fastdominant records poor in alpha activity, have notbeen confirmed. ' Immature' records are nomore common than in control groups (Hill, I957)though in catatonic stupor generalised 2 to 6c/s. activity may appear. The most strikingabnormalities are those reported by Hill (1957),who noted discharges of low amplitude bilaterallysynchronous slow activity, of fast spike and slowwave activity, or of multiple spikes, usually in thepost central areas, in 20 to 25% of cases (Fig. 5).Goldman (I959) has claimed that following therapid intravenous injection of ioo mg. thio-pentone sodium up to four times at intervals oftwo minutes, changes characteristic of schizo-

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(a) (b)FIG. 6.-Delirium due to bronchopneumonia. Female aged 6o years. (a) Delirium severe: frontally predominant high

voltage 2 c/s. runs. (b) One week later, moderately confused: bilateral delta activity evident, but of much loweramplitude.

phrenia appear. These include bilaterally syn-chronous theta activity with an amplitude of ioo,uV, persistent fast activity with an amplitudegreater than 25 FV and bursts of 25-100 ,lV fastactivity having a duration of 0.25 to i sec. Thiswork has not yet been confirmed.

Clouding of ConsciousnessClouding of consciousness is a symptom shared

by many conditions in which the function of thereticular activating system of the mid-brain anddiencephalon becomes impaired. This may resultfrom distortion of the blood vessels supplying theseareas, suddenly and catastrophically in headinjuries, or more insidiously due to raised intra-cranial pressure; to specific metabolic disordersresulting from certain vitamin deficiencies, uramia,cholkmia, hypoglycaemia and anoxia; or to theless well defined metabolic disturbances whichoccur in the deliria associated with infections andtoxic states.When clouding of consciousness occurs, what-

ever its cause, the EEG shows characteristicchanges. Sometimes these are associated withother abnormalities, if, for example, a focal cere-bral -disturbance ccexists. The presence of milddegrees of clouding of consciousness may often bevery difficult to establish on clinical grounds, andfrequently the EEG provides confirmatory- evi-dence of its existence. Even so, in the absence ofa previous EEG to establish the usual alpha fre-quency, it may be impossible to declare a recordabnormal, for the earliest change is a slowing of thealpha rhythm. If, for instance, this slows from I2

to 9 c/s., it will be abnormal for the individual,although it still falls within the somewhat arbitrarylimits of normality-8 to I3 c/s. Retrospectivelythe abnormality may be detected or confirmedwhen the patient's clinical state and EEG havereturned to their premorbid states. By the timeconfusion is evident clinically, the EEG as a rule istheta dominant, and in its distribution and responseto eye opening and closing, this theta activityoften behaves like the alpha rhythm. Withgreater impairment of consciousness, activity atlower frequencies becomes more prominent andless responsive. As coma ensues, delta activitybecomes dominant, and the record is made uplargely of i to 3 c/s. activity. This is generalizedthough often frontally predominant, bilaterallysynchronous and frequently tends to wax and wane(Fig. 6).Such EEG findings characterise the acute

meningitides and encephalitides, the encephalopathiesassociated with heavy metal poisoning, hypertension,acute porphyria, uracmia, anoxic states, severedegrees of adrenal and pituitary insufficiencyandhypoglycemia. In hepatic encephalopathy (portalsystemic encephalopathy) the same EEG patternappears when the blood ammonia level reaches200 to 400 ,ug./Ioo ml. Such changes may beprovoked or accentuated in patients with littlereserve of liver function by giving methionine or ahigh protein diet. In some stuporous cases, inaddition to the generalized slow activity, triphasicwaves become prominent. Each complex con-sists of two electro-negative waves separated by anelectro-positive wave of higher amplitude. Some-

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FIG. 7.-Raised intracranial pressure. Female aged 52 years with midline cerebellar tumour. Papillcedema marked,some clouding of consciousness: bilateral 2 C/s. runs of frontally predominant delta activity on a background ofmixed alpha and theta frequencies.

times these have quite a sharp outline and maythen resemble the complexes which accompanymyoclonic attacks (Bickford and Butt, 1955).

Psychiatric abnormalities are frequently presentin cases of pernicious aneemia and particularlycommon is the picture of a mild and reversiblesubacute organic reaction. EEG abnormalities-of the type characteristic of clouding of con-sciousness-are frequently present, though com-monly these too are only mild in degree (Walton,Kiloh, Osselton and Farrall, 1954).

In hypothyroidism reversible psychiatric andEEG abnormalities of a similar kind are oftenpresent. Usually the EEG tends to be of lowamplitude, and if hypothermia develops, itbecomes almost featureless (Nieman, 1959).

Raised Intracranial PressureSpace occupying lesions causing distortion of

the upper brain stem directly or indirectly by uncalherniation, frequently give rise to widespread EEGabnormalities. The correlation between the levelof intracranial pressure and these EEG abnor-malities is by no means close, but the evidence thatthe rise in pressure is responsible in the greatmajority of cases is very strong. Such a procedureas Torkildsen's operation, for instance, whichrelieves the raised pressure without influencing theunderlying lesion, can be expected to give rise toan improvement in both the level of consciousnessand in the EEG abnormalities. The abnormalitieshave the same characteristics as those described asaccompanying clouding of consciousness and areseen in purest form with infratentorial tumours.

The slow activity is commonly rhythmic andindeed almost sinusoidal (Fig. 7) but in; t5% ofcases is more irregular. Its distributiop -variessomewhat from case to case and though commonlygeneralized, it may be limited-for a,.time at anyrate-to the anterior, temporal or posterior regionsof the hemispheres. Moderate degrees of asym-metry are not uncommon but have no. localizingvalue (Daly, Whelan, Bickford and MacCarty,1953).

It has long been recognized that cerebraltumours may present initially with psychiatricdisorders. The latter do not always follow one ofthe classical organic patterns and if the picture isthat of a functional psychosis the possibility of anunderlying cerebral disorder may be overlooked.It is in such cases that the EEG may score a signalsuccess, for the finding of a localized focus of slowactivity may draw attention to the presence of theunsuspected space occupying lesion.A subdural hacmatoma is a variety of space

occupying lesion and the most characteristicclinical feature is fluctuation in the level of con-sciousness. The EEG may prove of great valuein the investigation of such a case, particularly if itpresents with a somewhat obscure psychiatricpicture. The EEG is almost always abnormal andin addition to generalized slow activity, there maybe a slow wave focus or an area of suppression ofelectrical activity over the lesion (Fig. 8).

Head InjuriesAlthough the EEG abnormalities following head

injury may be very varied in character and in

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A A A A A AFIG. 8.-Subdural hxematoma-right. Male aged 54 years. Right fronto-temporal slow activity with ipsilateral

suppression of alpha activity.

duration due to the great variety in the type, extentand distribution of the resulting lesions, it is the' diencephalic ischaemic syndrome ' (Dott, I960)that is responsible for both the impairment ofconsciousness and the accompanying generalizedEEG abnormalities. These too have the samefeatures as those associated with impaired con-sciousness due to other causes.

In very minor head injuries when consciousnessis lost for no more than a matter of seconds, thediffuse theta and delta activity which occur, dis-appear within a few minutes. Following moresevere injuries there may be relative suppressionof electrical activity for a period, particularly inthose cases whose prognosis is poor. Later slowactivity often at 4 to 6 c/s. appears and as recoveryensues, this shows a progressive increase in ampli-tude and frequency. Slow alpha activity appearsand gradually its frequency increases until itreaches its premorbid value. There is a roughcorrelation between the degree of abnormality ofthe EEG and the level of consciousness. (SeeDawson, Webster and Gurdjian, 195I.)Where localised cerebral damage has occurred,

the EEG is likely to show concomitant focalslow wave activity. Spikes or sharp waves arerarely seen in the acute phase but may appearlater.

The DementiasOld age is associated with a gradual decrease

in the amount, amplitude and frequency of thealpha rhythm, and there is a tendency for theamount of fast activity to be increased. There is

no increase in the amount of slow activity (Weinerand Schuster, 1956).The EEG abnormalities in senile dementia are

seldom striking, but a completely normal record isthe exception. The remaining alpha rhythm maybe slowed below 8 c/s. and this occurs against abackground of low amplitude, diffuse theta activitysometimes with delta components (Fig. ga). At alate stage the trace tends to be flat, lacking recog-nizable alpha or faster frequencies. In the simplepresenile dementias and in Huntington's chorea,similar patterns occur.The EEG in arteriosclerotic dementia also shows

the same characteristics although the abnormalitiesmay be somewhat more marked. Evidence of alocalized disturbance-usually a delta focus-isusual in cases with cerebral infarction.

In Alzheimer's disease and to a lesser extent inPick's disease, the incidence and severity oftheEEGabnormalities is very much greater. Little or noalpha rhythm survives and the record consists oflow to medium amplitude theta activity which isgeneralized and interspersed with runs of higheramplitude irregular delta activity which may befrontally predominant (Fig. gb) (Letemendia andPampiglione, 1958). The changes bear little re-lation to the severity of the dementia.There are a number of uncommon, patho-

logically distinct conditions which run a subacutecourse and are characterised by a progressivedementia, striking EEG abnormalities and ahopeless prognosis. In Jacob-Creutzfeldt's diseasebilateral sharp wave or sharp and slow wave dis-charges occur rhythmically and are accompanied

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(b)FIG. 9.-(a) Senile dementia. Male aged 82 years. Irregular theta components posteriorly, superimposed on low

voltage mixed alpha and beta frequencies. (b) Alzheimer's disease. Male aged 54 years. Irregular generalizedhigh voltage theta and delta activity.

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FIG. io.-Jakob-Creutzfeldt's disease. Female aged 63 years. Occasional bilateral spike discharges superimposed on abackground of generalized slow activity.

by myoclonic or choreiform movements. (Abbott,1959.) Initially the background record may benormal but soon it comes to be made up of thetaand delta activity (Fig. io). As the disease advancesthe amplitude of the sharp waves and of the back-ground activity diminishes, and the record becomesflat.

In subacute spongiform encephalopathy (Nevin,McMenemey, Behrman and Jones, I960) formerlyknown as Heidenhain's presenile dementia, thenormal rhythms diminish and disappear, beingreplaced by widespread high voltage slow activity

interspersed with bilaterally synchronous poly-phasic sharp wave complexes which occur re-petitively and sometimes rhythmically (Fig. ii).They are usually but not invariably symmetricaland are accompanied by myoclonic jerkings. Inmost cases these abnormalities are interspersedwith periods of low voltage slow activity whichmay also recur regularly. The abnormalities tendto increase as the disease progresses, but in theterminal phases the amplitude of the trace di-minishes and the sharp wave complexes disappear.

In subacuteprogressive encephalitis (Van Bogaert's

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FIG. I i.-Subacute spongiform encephalopathy. Female aged 70 years. Bilateral sharp and slow wave complexesoccurring periodically on a background of irregular slow activity.

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subacute sclerosing leucoencephalitis; subacuteinclusion body encephalitis of Dawson) progressiveslowing of the background rhythms occurs anddramatic high amplitude paroxysms of i to 3 c/s.activity appear, often with sharp components (Fig.12). Characteristically these are bilaterally syn-chronous, symmetrical and generalized, butexceptions occur. Once again the complexes areaccompanied by myoclonic jerkings. Progressionof the disease is associated with flattening of thebackground rhythms and ultimately with dis-appearance of the complexes.

In some cases of cerebral lipidosis in infants,changes of a similar kind are seen (Cobb, Martin

and Pampiglione, I952). Generalized high voltagetriphasic waves sometimes with a sharp appear-ance are superimposed on a background ofirregular i to 6 c/s. activity.The precise significance of the periodic dis-

charges in these various conditions is not known.It is generally believed that they are directlyrelated to the pathological changes in the cerebralcortex which are common to this group of dis-orders, but clearly they cannot be attributedmerely to degenerative changes. It is possible thatthe thalamic and brain stem reticular formationsplay some part in their genesis and spread. Notdissimilar periodic discharges sometimes occur

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FIG. 13.-Hypsarrhythmia. Male aged2ziyears with phenylketonuria. Generalized high voltage slow activity withrandom spike and slow wave discharges.

after attacks of grand mal, following head in-juries, in occasional cases of acute encephalitis andas the result of anoxic states following cardiacsurgery.

SubnormalityAs might be expected the incidence and variety

of EEG abnormalities in the subcultural group ofsubnormal individuals is much the same as in thegeneral population. It is to the pathologicalvarieties that one must look for gross abnormalities.

In congenital hydrocephalus, porencephaly,tuberous sclerosis, microcephaly and phenylketonuria,abnormal EEGs are usual. Many cases showbilateral spike or spike and slow wave activitywhich has its clinical counterpart in attacks ofepilepsy. In the latter two conditions the degreeof abnormality of the EEG may be sufficient to becalled hypsarrhythmia (Gibbs and Gibbs, I952).This is a purely descriptive term and is employedwhen the EEG is continuously abnormal showingwidespread multifocal spikes or spike and slowwave discharges against a background of diffuseirregular slow activity (Fig. I3). This pattern israrely seen after the age of 4 years. It is oftenassociated with 'salaam' attacks and almost in-variably with progressive organic deterioration.These cases form a group of varied ietiologythough natal or prenatal brain injury is thecommonest factor. The EEG abnormalities usuallydiminish markedly with age whilst the epilepticattacks but not the mental subnormality oftenrespond well to ACTH.

Temporal LobeEpilepsyThe estimate that 40% of all epileptics have focal

epileptogenic lesions in one or both temporal lobesmay well be a conservative one. The associationbetween epilepsy and a wide range of psychiatricdisorders has long been recognized and it is for themost part those patients with temporal lobeattack who are likely to develop epileptic per-sonality changes and psychoses.Many varieties of focal attack-or auras-have a

temporal lobe origin. Those of psychiatric origininclude brief experiences of depersonalisation,deja vu, fear or panic, depression or elation, as wellas hallucinations of smell, taste, hearing and vision.Psychomotor attacks, which are essentially briefperiods of clouding of consciousness in which thepatient is still capable of semi-purposive behaviour,are largely confined to these patients, as are themore prolonged episodes or ' twilight states '.Although a wide range of pathological condi-

tions involving the temporal lobe may give rise toepilepsy, in the great majority of cases the lesionsare atrophic and are situated on the medial aspectof one or both lobes. Many are due to birthinjury with uncal herniation (Earle, Baldwin andPenfield, I953). The medial aspect of thetemporal lobe is peculiarly sensitive to anoxia,and damage may consequently occur as a result of awide range of conditions including attacks of grandmal of centrencephalic origin (Scholtz, 1959).It also has the lowest threshold to electrical stimu-lation of any area of the cerebral cortex so that

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(a) (b)FIG. 14.-Temporal lobe epilepsy. (a) Male aged 34 years. Right mid-temporal spike focus.

'Mirror image ' anterior temporal spike and slow wave foci. (c) Male aged 42 years.anterior temporal sharp and slow wave focus, left mid-temporal spike focus.

(c)(b) Female aged 37 years.Independent foci: right

(a) (b)FIG. 15.-Temporal lobe epilepsy-recording with sphenoidal electrodes. (a) Right-sided spike focus confined to

sphenoidal leads. (b) Suppression of barbiturate induced fast activity in right fronto-temporal area, well shown insphenoidal leads.

scarring of this region is particularly liable to befollowed by epileptic seizures.

Interseizure PatternsThe most characteristic feature of the inter-

seizure EEG which indicates the presence of anepileptogenic lesion is a spike or sharp wave focus.The spikes are frequently associated with slowwaves (Fig. I4a). Occasionally the discharge con-sists of paroxysmal activity in the alpha, theta ordelta ranges. The paroxysmal epileptiform activityis often superimposed on a background of normalcortical rhythms, but often the lesion may give

other indications of its presence. Focal slowactivity, either continuous or fluctuating, is likelyin the case of a tumour, while particularly withextensive atrophic lesions, there may be an area ofdecreased amplitude of the cortical rhythms.Such a diminution of amplitude-sometimesreferred to as ' suppression '-is best demon-strated by injecting intravenous thiopentonesodium which induces widespread fast activity.In such cases this fast activity will be less evidentor even absent over the lesion (Fig. I5b) (Pam-piglione, 1952).The epileptiform discharges seen in cases of

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(a) (b)FIG. i6.-Psychomotor epilepsy-seizure pattern. (a) Before attack: generalized low amplitude slow activity. (b) During

attack: patient unresponsive, staring and salivating excessively. Bilateral high voltage rhythmical delta dischargewith some sharp components.

temporal lobe epilepsy are frequently bilateral.When this is so, they may occur independentlyindicating that both lobes are damaged; butfrequently the discharges are synchronous on thetwo sides-so-called ' mirror foci' (Fig. I4b). Inthis latter group the lesion may be unilateral andif the discharges are asymmetrical it is likely to beon the side of the higher amplitude sharp waves.When the discharges are of equal amplitude, itmay be impossible from a routine EEG to lateralizethe lesion, but asymmetry of barbiturate inducedfast activity may enable this to be done. The spikeor sharp wave discharges are often very inconstantand in a suspected case it may be necessary tocarry out several recordings in order to identifythem.A number of special techniques is employed to

aid diagnosis. As the lesion is deeply situated onthe medial aspect of the temporal lobe in somany cases, it is not surprising that little ornothing abnormal is detected by using ordinaryscalp electrodes. By directing a needle electrodethrough the mandibular notch below the zygomaticarch so that its tip lies close to the foramen ovale,electrical activity from the inferomesial aspect ofthe temporal lobe can be recorded (Fig. IS).A useful method of provoking epileptiform

activity is sleep. If the patient does not becomedrowsy spontaneously, sleep may be induced byany barbiturate or non-barbiturate hypnotic(Gibbs, 1958). Intravenous thiopentone sodiummay also be used and has the advantage that drug-induced fast activity may also be studied. Theactivation of the epileptogenic focus by intravenousleptazol, bemegride, chlorpromazine or imi-

pramine is also useful on occasion, and with theformer two drugs the investigation can be extendedin order to induce a convulsion. Unfortunately thevalue of such provocative techniques is severelylimited because so often these analeptic drugs giverise to bilaterally synchronous and symmetricaldischarges which provide no clue as to the later-alisation of the lesion.

Seizure PatternsThe usual EEG accompaniment of a focal

seizure is a train of focal spikes, sharp waves orspike and slow waves, which may remain strictlylocalized or spread widely in the same hemisphere.Sometimes the opposite hemisphere may also beinvolved. Immediately prior to the epileptiformactivity there may be some flattening of therecord. If the discharge and the attack remainlocalized, the epileptiform discharge will befollowed by normal rhythms or, for a period, bylow voltage random slow activity. Frequently thefocal seizure is followed by an attack of grand mal,in which case the focal discharge gives way tobilaterally synchronous spikes at 8 to I2 a second.

Should a psychomotor attack follow upon thefocal seizure, the EEG shows bilaterally syn-chronous discharges at 2 to io c/s.-usuallywithin the range 4 to 6 c/s.-which are mostevident in the fronto-temporal areas (Fig. i6).Only occasionally are there sharp wave com-ponents. In a few cases the psychomotor attack isaccompanied by generalized I4 to 20 c/s. activity,and in others the record merely shows a generaldiminution in amplitude. Rarely, no discerniblechange can be detected in the EEG. The bilateral

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distribution of the abnormalities in an attack ofpsychomotor epilepsy, together with the cloudingof consciousness which occurs, indicate involve-ment of the midline structures, although mostalways secondary to a temporal lobe attack.

In cases showing personality changes or epilepticpsychoses the temporal lobe abnormalities arecommonly bilateral. If dementia should ensue theepileptiform discharges become less frequent ordisappear, the alpha rhythm slows, often to below8 c/s. and low amplitude diffuse theta and deltaactivity becomes prominent.The term ' petit mal ' should be restricted to

brief absences occurring almost exclusively inchildren and accompanied by the characteristicbilaterally synchronous and symmetrical wave andspike discharge at 3 c/s. Rarely, prolonged epi-sodes of wave and spike discharge occur accom-panied by so-called ' petit mal status ' in which thechild becomes very disturbed, showing behavioursimilar to that seen in an attack of psycho-motor epilepsy (Zappoli, 1955).The occurrence of bilaterally synchronous

epileptiform discharges in both the interseizureand seizure patterns associated with focal lesionshas already been mentioned. This phenomenonis termed secondary bilateral synchrony and, thoughnot common, is most often seen with lesions of theinsular region or the medial aspect of one of thetemporal lobes. Sometimes the waveform may bevery similar to the wave and spike phenomenonseen in petit mal, and there is danger that thedischarges will mistakenly be regarded as centren-cephalic in origin. Rovit, Gloor and Rasmussen(I96I) have described a technique which enables adistinction to be made between these cases. Incases of centrencephalic epilepsy, the intracarotidinjection of 25 to ioo mg. amylobarbitone sodiumhas no effect upon the discharges, whereas incases of secondary bilateral synchrony such aninjection when made on the side of the lesion,abolishes the discharges over both hemispheres.Effects ofPhysical Treatments on the EEGE.C.T.

Following E.C.T. the patient's EEG is domi-nated by slow activity but returns to normal aftera variable period. After successive treatments theslow activity takes longer and longer to disappear.In the average patient when treatment is giventhree times a week, the abnormality becomespersistent after three or four treatments. The EEGconsists of generalized theta and delta activity,often frontally predominant, while the alphaactivity is diminished in amount and frequencyand may disappear. Clinically such a patient islikely to be confused. Roth (I95i) has shown thatfollowing E.C.T. slow activity is induced more

readily by intravenous thiopentone sodium andthat its amount has predictive value in relation tothe outcome with E.C.T. When followed up thosecases with more slow activity have the betterprognosis.

Prefrontal LeucotomyFollowing prefrontal leucotomy the EEG is

often dominated by high voltage, frontallypredominant delta activity which after a few weeksis replaced by theta activity. In most cases theEEG returns to its pre-operative state in aboutthree months. In cases where tension is relieved,there may be an increase in the amount of alpharhythm and a diminution in the amount of fastactivity.

HemispherectomyPatients suffering from infantile hemiplegia in-

cluding those with na?void amentia (Sturge-Kalischer-Weber syndrome) usually show dis-turbed behaviour in addition to fits and sub-normality. As a rule the EEG is grossly and con-tinuously abnormal. Although the lesion isunilateral, the EEG often shows bilateral spikeor spike and slow wave discharges on a back-ground of generalized delta activity. Followinghemispherectomy, the disturbed behaviour andfits may cease and the EEG may show a remark-able improvement. In spite of the absence of onehemisphere the EEG may be quite symmetricalthough more often there is some diminution inamplitude on the side of the operation.

ConclusionsIt is clear from the above account that although

certain psychiatric abnormalities are associatedwith interesting EEG changes, the clinical valueof electroencephalography to the psychiatrist islimited. So often, as in delirium, it merely providesadditional evidence to support what is alreadyclinically evident. In other cases, to the dis-appointment of the clinician, the EEG is reportedupon as normal or showing a non-specific abnor-mality. Even in indisputable cases of epilepsy,negative EEG findings are frequent, particularlywhen special techniques are not employed.Nevertheless, it is in epilepsy that the EEG hasits greatest value for in cases of cortical epilepsy,especially those with temporal lobe lesions, itprovides information which is unobtainable byany other method.Although of no value in the diagnosis of hysteria

it must be admitted that the EEG can on occasionbe of great value in creating doubt as to theaccuracy of such a diagnosis. Hysteria is such afrequent misdiagnosis when organic disorderspresent with bizarre behaviour; psychomotor

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January 1963 KILOH: The Electroencephalogram in Psychiatry 47

epilepsy, acute porphyria, attacks of spontaneoushypoglycaemia, Addison's disease, and cerebraltumour are examples of conditions that may beregarded as hysterical until the EEG findingsprompt rescrutiny of the clinical picture.

It is true of psychiatric cases, as of otherreferrals for EEG examination, that the clinicianshould have some knowledge of what electroence-phalography has to offer and particularly be

aware of the limitations of the method. Onlywhen full clinical details of the case are availablecan adequate interpretation be attempted and inaddition to supplying thpse, it is highly desirablethat the clinician should pose a precise questionto which he requires an answer. When an EEG andits accompanying referral form are scrutinized itmust be admitted that often one learns more aboutthe clinician than the patient.

REFERENCESABBOTT, J. (1959): The EEG in Jakob-Creutzfeldt's Disease, Electroenceph. clin. Neurophysiol., iI, I84.ACKNER, B., and PAMPIGLIONE, G. (I959): An Evaluation of the Sedation Threshold Test, J. psychosom. Res., 3, 271.BICKFORD, R. G., and BUTT, H. R. (I955): Hepatic Coma: The Electroencephalographic Pattern,J. clin. Invest., 34, 790.COBB, W., MARTIN, F., and PAMPIGLIONE, G. (1952): Cerebral Lipidosis: An Electroencephalographic Study, Brain,

75, 343-DALY, D., WHELAN, J. L., BICKFORD, R. G., and MACCARTY, C. S. (1953): The Electroencephalogram in Cases of

Tumours of the Posterior Fossa and Third Ventricle, Electroenceph. cin. Neurophysiol., 5, 203.DAVIS, P. A. (I939): Evaluation of the Electroencephalogram of Schizophrenic Patients, Amer. J. Psychiat., 96, 85I.DAWSON, R. E., WEBSTER, J. E., and GURDJIAN, E. S. (1951): Serial Electroencephalography in Acute Head Injuries,

J. Neurosurg., 8, 6I3.DITMAN, K. S., and BLINN, K. A. (1954-55): Sleep Levels in Enuresis, Amer. Y. Psychiat., III, 9I3.DOTT, N. M. (I960): Brain, Movement and Time, Brit. med. J., ii, 12.EARLE, K. M., BALDWIN, M., and PENFIELD, W. (1953): Incisural Sclerosis and Temporal Lobe Seizures Produced

by Hippocampal Herniation at Birth, Arch. Neurol. Psychiat. (Chicago), 69, 27.GIBBS, F. A., and GIBBS, E. L. (1952): 'Atlas of Electroencephalography ',Vol. 2. Epilepsy. (a) 329, (b) 24. Cambridge,

Mass.: Addison-Wesley Press.(1958): Abnormal Electrical Activity in the Temporal Regions and its Relationship to Abnormalities of Behaviour,Res. Publ. Ass. nerv. ment. Dis., 36, 278.

GOLDMAN, D. (1959): Specific Electroencephalographic Changes with Pentothal Activation in Psychotic States,Electroenceph. clin. Neurophysiol., II, 657.

HILL, D. (1952): EEG in Episodic Psychiatric and Psychopathic Behaviour, Ibid., 4, 419.(1957): The Electroencephalogram in Schizophrenia, in ' Schizophrenia: Somatic Aspects ', p. 33. Ed. byD. Richter. London: Pergamon Press.

LETEMENDIA, F., and PAMPIGLIONE, G. (1958): Clinical and Electroencephalographic Observations in Alzheimer'sDisease, J. Neurol. Psychiat., 21, I 67.

NEVIN, S., MCMENEMEY, W. H., BEHRMAN, S., and JONES, D. P. (I960): Subacute Spongiform Encephalopathy: ASubacute Form of Encephalopathy Attributable to Vascular Dysfunction (Spongiform Cerebral Atrophy), Brain,83, 519.

NIEMAN, E. A. (1959): The Electroencephalogram in Myxcedema Coma: Clinical and Electroencephalographic Studyof Three Cases, Brit. med. Y., i, 1204.

NYMGAARD, K. (1959): Studies on the Sedation Threshold, Arch. gen. Psychiat., I, 530.PAMPIGLIONE, G. (1952): Induced Fast Activity in the EEG as an Aid in the Location of Cerebral Lesions, Electroenceph.

clin. Neurophysiol., 4, 79.REFSUM, S., PRESTHUS, J., SKULSTAD, A., and OSTENSJ6, S. (I960): Clinical Correlates of the I4 and 6 per second

Positive Spikes, Acta psychiat. scand., 35, 330.ROTH, M. (I95I): Changes in the EEG under Barbiturate Anaesthesia Produced by Electro-convulsive Treatment and

their Significance for the Theory of ECT Action, Electroenceph. clin. Neurophysiol., 3, 26I.RovIT, R. L., GLOOR, P., and RASMUSSEN, T. (I96I): Intracarotid Amobarbital in Epileptic Patients, Arch. Neurol.

(Paris), 5, 6o6.SCHOLZ, W. (1959): The Contribution of Patho-anatomical Research to the Problem of Epilepsy, Epilepsia, I, 36.SHAGASS, C. (1954): The Sedation Threshold: A Method for Estimating Tension in Psychiatric Patients, Electroenceph.

clin. Neurophysiol., 6, 221., and JONES, A. L. (1958): A Neurophysiological Test for Psychiatric Diagnosis: Results in 750 Patients, Amer.J. Psychiat., 114, roo2.

WALTER, R. D., COLBERT, E. G., KOEGLER, R. R., PALMER, J. 0., and BOND, P. M. (I960): A Controlled Study of theFourteen- and Six-per-second EEG Pattern, Arch. gen. Psychiat., 2, 559.

WALTON, J. N., KILOH, L. G., OSSELTON, J. W., and FARRALL, J. (1954): The Electroencephalogram in PerniciousAnmemia and Subacute Combined Degeneration of the Cord, Electroenceph. clin. Neurophysiol., 6, 45.

WEINER, H., and SCHUSTER, D. B. (1956): The Electroencephalogram in Dementia: Some Preliminary Observationsand Correlations, Ibid., 8, 479.

WILLIAMS, D. (1941): The Significance of an Abnormal Electoencephalogram, J. Neurol. Psychiat., 4, 257.ZAPPOLI, R. (1955): Two Cases of Prolonged Epileptic Twilight State with Almost Continuous 'Wave-Spikes',

Ibid., 7, 421.



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THE ELECTROENCEPHALOGRAM IN PSYCHIATRY · Electroencephalography and Clinical Neurophysiology.) (b) Percentage distribution of sedation thresholds in mg./kg. body weight for psychotic