Electroencephalography in Neuropsychiatry

April 1, 2006

The recent evolution of neuropsychiatry/behavioral neurology as a subspecialty represents a paradigmatic shift regarding the responsibility of psychiatrists in diagnosing and managing behavioral disorders with concomitant and demonstrable brain pathology such as dementia or head injury. This authors define the clinical usefulness of electroencephalography in evaluating neuropsychiatric disorders.

Special Report: Neuropsychiatry

Electroencephalography (EEG) isa noninvasive, widely available,and relatively inexpensive testthat can help exclude or identify structuralor functional factors contributingto psychiatric syndromes. This articledefines the clinical usefulness of EEGin evaluating neuropsychiatric disorders,emphasizing the complementarynature of the visually inspected standardEEG (SEEG) and the computeranalyzedquantified EEG (QEEG).

The recent evolution of neuropsychiatry/behavioral neurology as asubspecialty linking these formerlydisparate fields represents a paradigmaticshift regarding the responsibilityof psychiatrists in diagnosing andmanaging behavioral disorders withconcomitant and demonstrable brainpathology such as dementia or headinjury. In addition, the biologic underpinningsof many mental illnesses,including bipolar disorder and depression,are now described in terms of theiranatomy and physiology. QEEG analysis increases the sensitivity of EEG tophysiologic or pathologic changes associatedwith such disorders.

Standard EEG

SEEG refers to the visual analysis ofongoing voltage recordings from multiplescalp locations. Two types of EEGdeviations are usually indicative ofsignificant cerebral pathology. The firstis paroxysmal activity, including sharpwaves, spikes, and episodic slowwaves, indicating episodic abnormalneuronal discharges. These can befocal, suggesting structural pathology,or bilateral and more suggestive offunctional pathology. The second typeof EEG deviation is sustained slowingof normal brain rhythms. Slowing alsocan be diffuse, indicating more generalizedpathology, or focal, indicatinga localized pathology.

The most frequent reason for an EEGreferral is to exclude a general medicalcondition, such as delirium, or a specificneurologic problem, such as epilepsy,as a cause of or a contributing factor tothe presenting symptoms. Since the useof routine test batteries to exclude medical conditions is costly,clinicians must rely primarilyon 2 red flags to trigger organicworkups: unusual presentationsand atypical age at onset. Theyield is consistently low whenusing neuroevaluative tests touncover causes such as tumorsor aneurysms for syndromespresenting without manifestneurologic disturbances. It ismuch more likely that an EEGwill uncover a factor that maybe contributing to, but does notnecessarily fully explain, thesyndrome. It may also be helpfulin revealing a factor thatcould help guide treatment,such as temporal lobe spiking in panicdisorder.1

Quantified EEG

After the EEG has been recorded andvisually interpreted by the electroencephalographer,it may be analyzedfurther using quantitative means.2QEEG analysis is always a post hocprocedure done after visual interpretationof the SEEG by a qualified electroencephalographer. It is specificallynot recommended for use clinically asa stand-alone procedure. At its mostbasic level, QEEG provides a methodof calling the electroencephalographer'sattention to aspects of the original EEGrecord that may have been overlooked.QEEG's quantitative nature makes itexquisitely sensitive to subtle frequencychanges and to abnormalities in the coherence of activity within and amongbrain regions.

Brain activity varies among healthypeople, and normal variability must bedistinguished from that outside the normalrange. An underlying assumption is thatthe more unusual the patient's brain activitycompared with that of normal persons,the more likely it is that the statisticalabnormality represents pathology. Theestablishment of normal limits is greatlyaided by quantitative analysis comparingthe patient's QEEG with those derivedfrom large groups of healthy persons.Brain activity also changes with age, andQEEG tracks the moving window of normallimits across the entire life span.

In addition, QEEG can help the physicianarrive at a specific diagnosis.Patients who have known neuropsychiatricdisorders often show characteristicQEEG profiles, distinguishing themfrom patients who have similar disorders.When facing a difficult diagnosticquestion, the physician can comparethe patient's QEEG with the profilescharacteristic of the different diagnosticpossibilities, looking for the best fit.An extensive body of research showsthat the accuracy of such computerizeddiagnostic classifications on the basisof QEEG alone typically exceeds 80%,although in an actual clinical setting thephysician always makes the diagnosis,informed by other sources of informationin addition to QEEG. Well-replicatedstudies have demonstrated QEEGclassification accuracies high enough tobe useful in diagnosing learning andattention disorders in children, and mooddisorders (including bipolar disorder)and dementia among adults.3

Clinical Indications

The relative usefulness of SEEG andQEEG depends on the clinical indicationsfor testing. Mental status changes,unusual presentations, personalitychanges, episodic behavior, and attentionproblems are situations that oftenprompt testing.

Acute or gradualmental status change

Patients with advanced dementia rarelyhave normal SEEG results, so a normalEEG is important in diagnosing pseudodementiasecondary to depression orpsychosis. When dementia and depressioncoexist, it becomes important toassess the relative contribution of eachdisorder to the overall clinical presentation;and SEEG has been shown to behelpful in this situation.4 SEEG is insensitiveto the early stages of dementia,however, and cannot be relied on indiagnosing frontotemporal dementia(FTD).

One reason for SEEG insensitivityto early dementia is that EEG changesin most dementing disorders are exaggerationsof those found in normalaging. QEEG controls for healthy aging,however, and is sensitive even to subtlechanges beyond normal limits. QEEGdetects significant abnormalities at theearliest stages of dementia, whichincrease in parallel with increasingdementia severity. Figure 1 shows anexample of a QEEG obtained from ademented patient. In addition to themore easily identified dementia types,QEEG may facilitate the difficult diagnosisof FTD. Perhaps of more importance,QEEG has been shown todistinguish accurately between dementiaand pseudodementia.

The differential diagnosis of acutelydisturbed and disorganized dementedor psychotic patients often includesdelirium. SEEG may be helpful inrevealing whether altered consciousnessis the result of a diffuse encephalopathicprocess, a focal brain lesion, or continuedepileptic activity without motormanifestations. Usually, delirious patientshave a toxic-metabolic encephalopathywith diffuse slowing of thebackground rhythms. Figure 2 showsan SEEG obtained from an acutelyconfused patient. Limited publishedresearch, however, suggests that QEEGadds little to standard visual analysisfor the detection of delirium.

Unusual presentation

An atypical clinical presentation is themost important factor for initiating anSEEG evaluation.5 However, patientswith a nonatypical rapid-cycling bipolardisorder also may exhibit epileptiformEEG discharges.6 This mayexplain the reported effectiveness ofanticonvulsants for rapid-cycling bipolardisorders.

Himmelhoch7 described the clinicalcharacteristics of “subictal mood disorders,”including brief euphorias, mixedbipolar episodes, brief severe depressivedips with impulsive suicide attempts,compulsive symptoms, irritability andhostile outbursts, and marked premenstrualworsening. Patients with thesedisorders may also have paradoxicalreactions to lithium and antidepressants,with better response to anticonvulsants.

QEEG is very sensitive for the detectionof depression and for the discriminationbetween depression anddementia. A limited number of articlesin the literature further suggest thatQEEG accurately discriminates betweenunipolar depression and bipolar disorder,but this finding awaits independentreplication.

Recent personality change

An obvious recent personality changeshould always be viewed as a dangersign, and a full evaluation shouldbe performed. Chronic postconcussivesyndrome deserves special mention.QEEG is more helpful than SEEG insuch cases. Even mild concussions inwhich the patient experiences either noloss of consciousness or less than 20minutes of unconsciousness can causereduced attention span, reduced shorttermmemory capacity, depression, mood disorders, word-finding problems,and slowness of thought. EEGchanges that often accompany mildhead injury include reduced beta and/oralpha activity and increased theta activity.8 One commercially available QEEGsystem is tailored to detect brain damage secondary to closed head injuries andhas been demonstrated to do so withgreater than 95% accuracy.9

Episodic behavior

Case reports have described patientsin whom borderline personality disorder(BPD) was diagnosed but who weresubsequently found to have complexpartial seizures documented by epilepticdischarges over temporal regions.10 The prevalence of abnormal EEGsamong clinic populations ranges from6.6% in patients with rage attacks andepisodic violent behavior to 53% inpatients with antisocial personality disorder.11,12 A flowchart for evaluation ofpatients presenting with episodic aggressivebehavior is shown in Figure 3.

Whether an abnormal EEG predictsa favorable therapeutic response to anticonvulsantsis currently unknown.Anticonvulsants can block epileptiformdischarges and can lead to dramatic clinicalimprovement in persons exhibitingrepeated and frequent aggression.13 Theaddition of carbamazepine to the treatmentregimen of patients with schizophreniawho also exhibit EEG temporallobe abnormalities but no history ofseizure disorder can be beneficial.14 Anticonvulsants also may reduceaggressive tendencies irrespective ofEEG abnormalities.15

Finally, panic symptoms resemblesymptoms induced by temporolimbicepileptic activity, particularly that originatingfrom the sylvian fissure. Panicdisorder is the most common psychiatricdisorder that must be differentiatedfrom temporal lobe epilepsy.16

Attention and learning disorders

Frank17 reported that 21 (31%) of asample of 64 children with attentiondeficit/hyperactivity disorder had abnormalSEEG. Of these, 84% had spikesor spike-wave discharges. Hughes andassociates18 found “definite noncontroversialepileptiform activity” in 53(30.1%) of 176 children with ADHD.Mainly focal and usually occipital ortemporal, the epileptiform activity was less often generalized, with bilaterallysynchronous spike and wave complexesseen in 7% of children.

Several large, independently replicatedstudies have shown that QEEGdistinguishes between healthy childrenand those who have a variety ofattention or learning disorders, withaccuracies typically exceeding 80%.While autism cannot be diagnosedbased on EEG findings, an EEG canhelp rule out the presence of epilepticactivity that is relatively common inthis group.

Adequate SEEG evaluation

For an adequate SEEG evaluation, theclinical reason for the referral must beconsidered. If a slow-wave abnormalityis suspected, an awake recording issufficient. The most important caveatis to make absolutely sure that the patientis alert during the procedure. Inpatients with borderline results, theinclusion of hyperventilation couldenhance the abnormality.

If the purpose of SEEG is to rule outepileptiform discharges, an awake EEGis inadequate, and the inclusion of asleep tracing is important. The EEGreport should clearly indicate the stageof sleep during the recording. Serialrecordings enhance the likelihood offinding abnormalities, particularlyepileptiform abnormalities.19 In ourexperience, the yield of more than 2recordings does not justify the addedexpense. The second recording may beperformed following sleep deprivation.

Adequate QEEG evaluation

As a post hoc analytic procedure, QEEGis supplementary and complementary toSEEG. No special recording proceduresare required other than ensuring thatfilters and sampling rates are set at specifiedlevels. Virtually all modern EEGmachines can provide a digitized recordsuitable for computerized analysis.Because QEEG analysis is easily biasedby artifacts, the electroencephalographerbegins by selecting artifact-free samplesof the alert eyes-closed SEEG, whichthen are analyzed mathematically usingcommercial software. Abnormalities detectedby QEEG are traced back to theoriginal SEEG and interpreted by theelectroencephalographer.

When using QEEG to assist in diagnosis,the physician again plays thecentral role of narrowing the diagnosticpossibilities to a small number(usually 2). The more the physicianknows about the patient, the more alternativediagnoses can be excluded,increasing the accuracy of the classification.QEEG is not used as a diagnosticfilter, running the patient's datathrough all possible classifiers. Suchmisuse nearly always produces spuriousresults.

Problems encountered in QEEGgenerally reflect user error. Incorrectlyset filters, unrecognized patient drowsinessor artifacts, and other recordingor screening errors can be prevented bythorough training and the maintenanceof high laboratory standards. Specifictraining is required to correctly useQEEG software and to interpret theresults. All use of QEEG must be supervisedby an electroencephalographer,and its application to psychiatric diagnosisrequires additional expertise in theDSM differential diagnostic criteria.

SEEG and QEEG are complementarytechniques, and modern digitalequipment facilitates and tends to lowerthe cost of QEEG. Specialized trainingis necessary to interpret both SEEG andQEEG, and the interpreter must beproficient in psychiatric differentialdiagnosis.

Dr Boutros is professor of psychiatry and neurologyat the Wayne State University School ofMedicine in Detroit, as well as director of theneuropsychiatry division and clinical electrophysiologylaboratories. He reports that he hasno conflicts of interest regarding the subjectmatter of this article.
Dr Coburn is professor and director of researchin the department of psychiatry andbehavioral sciences at the Mercer UniversitySchool of Medicine, Macon, Ga. He reportsthat he has no conflicts of interest regardingthe subject matter of this article.

References:

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