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Computer-analyzed quantitative EEG findings in Capgras syndrome

Roy Reeves, DO, PhD

Jackson VA Medical Center, University of Mississippi School of Medicine, Department of Psychiatry, Jackson, MS, USA

Randy Burke, PhD

Jackson VA Medical Center, University of Mississippi School of Medicine, Department of Psychiatry, Jackson, MS, USA

KEYWORDS: quantitative EEG, Capgras syndrome, EEG


TO THE EDITOR: Capgras syndrome (CS) is a misidentification syndrome characterized by the transient, recurrent, or permanent belief that someone known to an patient has been replaced by an imposter with a strong physical resemblance. CS has been observed in association with schizophrenia, schizoaffective disorder, dementia, and neurologic disorders. Neuroanatomical evidence shows that lesions in the right hemisphere are common among patients with CS; bilateral damage also has been found in many patients.1 Investigations involving visually analyzed EEGs have not revealed characteristic findings for patients with CS; in an analysis of 13 CS cases,2 only 4 had definite EEG abnormalities, while another analysis of 9 cases3 reported 7 patients as having normal EEGs. Forstl et al4 reviewed the EEGs of 59 CS patients; 31 (59%) demonstrated non-focal slowing of background activity, 5 (8%) right focal abnormalities, and 10 (17%) left focal abnormalities.

Using a MEDLINE search we could find no previous investigations of computer-analyzed quantitative EEG (QEEG) in CS. In this institutional review board-approved preliminary study QEEGs and MRIs were obtained for 15 patients with CS. Cognitive evoked potentials (P300) also were recorded when possible. All patients selected for this study had permanent CS (ie, their misidentification delusions never remitted), had been admitted to a psychiatric unit within the 48 hours preceding the study, and had been off medications for at least a week (eliminating the likelihood of a medication affecting the EEG). Each patient was diagnosed with schizophrenia, and was psychotic at the time of hospitalization. Patients with neurologic conditions capable of affecting EEGs were excluded from the study. Use of these stringent guidelines provided criteria that eliminated many confounds that could occur with CS patients, and created a standard which rarely was met, resulting in a small but refined cohort of patients.

Compared with EEG results reported in previous studies, QEEGs appeared to be more sensitive and detected more abnormalities, but results overall were somewhat inconsistent (TABLE). Three patients had normal findings; 4 patients had generalized or non-focal abnormalities that did not demonstrate unequivocal lateralization to either hemisphere; 3 patients had notable abnormalities in the right hemisphere, and 2 others had right-sided abnormalities plus other nonlocalized findings. Two patients had left-sided abnormalities and other nonlocalized findings, and 1 patient had focal abnormalities in both hemispheres along with generalized abnormalities. In spite of more patients having primarily right hemispheric lesions (5) than left hemispheric lesions (2), a reliable QEEG finding does not emerge. For many patients, P300 data shows longer latencies than would be expected in normal individuals, a result that has been found in previous investigations.5 Cognitive visual evoked potentials appear to be more affected than auditory evoked potentials; this observation could be consistent with visual processing impairment, but the small number of patients who completed this task does not allow for definite conclusions.


Quantitative EEG, P300 auditory and visual evoked potentials, and MRI findings of 15 patients with Capgras syndrome

Age/sex Focus of delusion QEEG results P300 VEP latency (msec) P300 AEP latency (msec) MRI findings
41 M Mother Decreased alpha frequency and delta absolute power bilaterally; decreased theta interhemispheric coherence, centroparietal 550 335 Normal
46 F Siblings Increased theta absolute power, right frontal area Uncooperative Uncooperative Normal
37 M Wife, friends Decreased alpha and increased theta frequency, all areas; decreased delta and beta relative power, right frontal area; decreased delta interhemispheric coherence, left centroparietal; decreased delta intrahemispheric coherence, frontal and occipital areas Not seen 328 Mild atrophy
32 M Wife Normal 458 324 Normal
49 F Father Increased beta relative and absolute power, frontal areas bilateral 446 334 Normal
55 F Husband, children Decreased alpha frequency and increased delta absolute power, right frontal 495 346 Mild atrophy
60 M Wife Normal 475 342 Normal
52 M Multiple persons Decreased alpha frequency, frontal bilateral; increased delta absolute power, right frontal 547 370 Normal
34 F Children Decreased alpha frequency all areas; increased theta and delta absolute power, all areas, greatest frontocentral; decreased interhemispheric coherence, centroparietal 593 417 Small right parieto-occipital lesion
63 F Husband Decreased alpha and theta absolute power all areas, maximal frontal; decreased alpha and theta interhemispheric coherence, several areas; decreased alpha intrahemispheric coherence, frontal and left occipital areas Not seen Not seen Normal
43 M Family Increased mean theta frequency, frontocentral areas; decreased delta absolute power bilaterally; decreased theta interhemispheric coherence, left frontotemporal Not seen 326 Normal
42 M Neighbor Decreased alpha frequency, bilateral frontotemporal Uncooperative 349 Normal
60 F Husband Decreased alpha frequency, right frontotemporal Not seen 370 Mild atrophy
41 F Children Decreased alpha frequency and increased theta relative power, bilateral; increased theta absolute power, posterior area; increased delta absolute power, right temporal/occipital region; decreased delta, theta, and alpha interhemispheric coherence, several areas 554 305 Normal
42 M Wife Normal Uncooperative Uncooperative Normal

Although previous studies have shown that patients with CS often have right hemispheric lesions, many CS patients also have been noted to have bilateral lesions.1 Therefore, a variety of QEEG findings is not surprising. In summation, there do not appear to be specific QEEG findings consistently associated with CS in this preliminary pilot study. However, further research using multiple diagnostic modalities could prove beneficial.

DISCLOSURES: The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.


  1. Bourget D, Whitehurst L. Capgras syndrome: a review of the neurophysiological correlates and presenting clinical features in cases involving physical violence. Can J Psychiatry. 2004;49:719–725.
  2. Kirakos R, Anath J. Review of 13 cases of Capgras Syndrome. Am J Psychiatry. 1980;137:1605–1607.
  3. Huang TL, Liu CY, Yang YY. Capgras syndrome: analysis of nine cases. Psychiatry Clin Neurosci. 1999;53:455–459.
  4. Forstl H, Almeida OP, Owen AM, et al. Psychiatric, neurological and medical aspects of misidentification syndromes: a review of 260 cases. Psychol Med. 1991;21:905–910.
  5. Jeon YW, Polich J. Meta-analysis of P300 and schizophrenia: patients paradigms, and practical implications. Psychophysiology. 2003;40:684–671.

CORRESPONDENCE: Roy R. Reeves, DO, PhD, VA Medical Center, 1500 E. Woodrow Wilson Drive, Jackson, MS 39216 USA, E-MAIL: roy.reeves@va.gov