Language: Spanish
References: 56
Page: 173-181
PDF size: 158.09 Kb.
ABSTRACT
The obsessive compulsive disorder (OCD) is a diverse and multidimensional psychiatric syndrome, characterized by obsessions and compulsions, where anxiety is considered to be a key clinical component. Imaging studies have shown brain abnormalities in patients with OCD involving mainly the frontotemporal circuits, the orbitofrontal and the anterior cingulate cortex. These techniques have a high spatial resolution to identify brain alterations in this disorder but have less time resolution and are more expensive than electrophysiological studies. The electroencephalogram (EEG) and event-related potentials (ERPs) are the most common electrophysiological techniques used in the research of OCD. The EEG represents the electrical activity of the brain as recorded by electrodes placed on the scalp. The ERPs are voltage fluctuations that are temporarily linked to the presence of a physical or mental event. The best-known type of EEG is the «traditional EEG» (analyzed by visual inspection), which is characterized by the presence and topographic distribution of four frequency bands: delta (δ), theta (θ), alfa (α), and beta (β). The δ and θ bands are identified as slow activities while the α and β bands are known as fast activities. The slow activity has been referred to as the most common abnormality in OCD, specially in the θ band. Moreover, the Broad Band Spectral Parameters (BBSPs) have contributed, for more than two decades, to the study of psychiatric patients and their values can be presented in a compact form as a topographic map on the scalp (Brain Mapping in the frequency domain).
The Absolute Power (AP) and the Relative Power (RP) are the most common BBSPs used. Is difficult to determine if AP is abnormal at certain age due to the fact that AP values vary with age. To solve it, it is suggested to transform AP’s values, in every band, into Z values which indicate how close is the subject to the average values of normal individuals of the same age. Since abnormal increases and decreases have been described in the anterior brain regions by the slow bands (δ and θ) and the fast bands (α and β), some authors have considered inconsistent the alterations that have been observed with the BBSPs.
Nevertheless, in accordance with traditional EEG studies, other authors have confirmed the excess of theta activity in patients with OCD. Of special interest for the clinical practice is that some authors have demonstrated, using the BBSPs, the existence of two OCD patients subgroups, which were homogeneous from the clinical point of view: one group with an excess of θ in the RP values, specially in the frontal and fronto-temporal regions, and a significative increase of α RP values for the other group. Eighty per cent of the patients of the first subgroup did not improved with selective serotonine reuptake inhibitors treatment, whereas 82.4 % of the patients of the second group improved. These results were confirmed ten years later and the α RP excess, present in those patients who improved, decreased after three months of treatment. However, it must be reminded that the generator of abnormal brain electrical activity, could be originate in a distant place to the location shown by the scalp electrodes.
LORETA and VARETA are two methods used to calculate the origin of the generators above mentioned. The first investigation using LORETA was published in 2005, and it was observed that compared to controls, the OCD group showed an excess of β activity in the cingulate gyrus (mainly in the middle cingulate gyrus), as well as in the adjacent frontal, parietal and occipital regions. Two years later, in another EEG sources study, but using VARETA, has been found an excess of α activity with abnormal EEG sources located in the striatum and in the orbito-frontal and temporo-frontal regions, which decreased after successful treatment with paroxetine.
Therefore, it is also heartening to confirm, through the study of generators of the EEG, a result of great clinical value previously proved with BBSPs.
The ERPs are divided into two types: exogenous and endogenous. In this paper we shall refer to the endogenous or cognitive type which depends on the nature of the interaction between the subject and the stimulus, so it will vary with attention, relevance of the task and the processing required. The ERPs are small voltage fluctuations that are identified by their latency (time of appearance in milliseconds), its amplitude (voltage in microvolts) and its polarity (positive or negative voltage).
Among the most characteristic ERPs components are the N200 and the P300. In most cases these components are elicited through a classical «oddball» paradigm, in which an infrequent stimulus («target») is randomly interspersed within an ongoing train of a different repeating stimulus («standard»). There are at least two subcomponents of the P300: a frontal/central maximum amplitude component, the P3a that appears after the occurrence of unexpected distracters, regardless of its relevance for the task and represents an orienting response. The other one is the P3b, which has been more studied, it has a central/parietal distribution and evaluates attention and working memory.
The N200 component has been linked to the automatic and voluntary process of identification and categorization of the stimuli. In patients with OCD there have been described shorter latencies and larger amplitudes for the P3b and N200 components, suggesting hyperarousal of the cortex and overfocused attention. However, there have also been described shorter amplitudes and larger latencies for the P300 component in the frontal regions, which have been related to an impairment of working memory or attention. Some authors have observed an inverse correlation between the N200 amplitude and the severity of the symptoms as well as a positive correlation between this variable and the response to treatment with selective serotonine reuptake inhibitors, but others have pointed out that patients that respond to treatment have a lower N200 amplitude, a larger P300 amplitude and a N200 and P300 shorter latencies.
As for the possible association between the ERPs and the disease’s evolution time, there has been a positive correlation between the N200 amplitude and the chronicity of the disorder. It has also been found that the amplitude of the P300 component is positively associated with the severity of symptoms assessed by the Yale-Brown obsessive compulsive scale.
Finally, it can be considered that, from a clinical point of view, patients with OCD have the feeling that «something is not right» or «of having committed an omission» when it has not been committed, and «get caught» on excessive verification responses when an error mistake has happened. That phenomenological consideration has been associated to an alteration of the action monitoring process, which represents one of the executive functions mediated by the frontal regions, particularly the anterior cingulate cortex, which may be «hyperactive» in OCD patients when they have the feeling of having made a mistake. The action monitoring process has been evaluated in patients with OCD through an ERP component called «Error-related Negativity» (ERN). The ERN is a negative wave around the 50-150 ms, which appears after the subject committed an error or thinks it has been done. In an ERN study it was found greater ERN amplitudes in the frontal regions in subjects with high obsessivity rates compared to subjects with low obsessivity ones, which is consistent with the hyperactivity hypothesis of the fronto-temporal system proposed for this disorder and is according to the theory that patients with OCD show an increase of the monitoring function when a mistake has been done.
However, there are authors who have not found differences in the NRE between healthy subjects and patients with OCD under pharmacological treatment, but they have observed a significant negative association between the ERN amplitude and the severity of the disorder. Hajcak et al. 2008, noticed an amplitude ERN increase in a group of subjects with pediatric OCD compared with the control group, which is consistent with ERN adult studies. In addition, since the ERN was not associated with the symptom severity or the response to treatment with cognitive behavioral therapy, that is why this alteration of the ERN could be a trait-like marker. Based on the foregoing, these researchers suggested that the increase in the amplitude of the NRE could be considered as an endophenotype. The EEG and ERPs can do an important contribution, in conjunction with clinical and imaging studies, to the identification of the structures and circuits involved in the pathophysiology of OCD. In addition, there are several evidences to support the utility of these electrophysiological techniques as complementary studies in the clinical evaluation and treatment of patients with OCD.
REFERENCES
Attiullah N, Eisen JL, Rasmussen SA. Clinical features of obsessive-compulsive disorder. Psychiatr Clin North Am 2000;23(3):469-91.
Anderson KE, Savage SR. Cognitive and neurobiological findings in obsessive– compulsive disorder. Psychiatr Clin North Am 2004;27(1):37-47.
Szeszko PR, Ardekani BA, Ashtari M, Malhotra AK, Robinson DG et al. White matter abnormalities in obsessive-compulsive disorder: a diffusion tensor imaging study. Arch Gen Psychiatry 2005;62(7):782-790.
Valente AAJR, Miguel EC, Castro CC, Amaro EJR, Duran FL et al. Regional gray matter abnormalities in obsessive-compulsive disorder: a voxel-based morphometry study. Biol Psychiatry 2005;58(6):479-487.
Picton TW, Bentin S, Berg P, Donchin E, Hillyard SA et al. Guidelines for using human event-related potentials to study cognition: recording standards and publication criteria. Psychophysiology 2000; 37(2):127-152.
Prichep LS, Mas F, Hollander E, Liebowitz M, John ER et al. Quantitative electroencephalographic subtyping of obsessive-compulsive disorder. Psychiatry Res 1993;50(1):25-32.
Ricardo-Garcell J. Clinical homogeneity vs EEG heterogeneity in psychiatric illness. Attention Deficit Hyperactivity Disorder a good example. Guadalajara, Mexico: International Meeting of Mind & Electrophysiology; 2005; p 265-266.
Pacella BL, Polatin P, Nagler SH. Clinical and EEG studies in obsessivecompulsive states. Am J Psychiatry 1949;100:830-838.
Insel TR, Donnelly EF, Lalakea ML, Alterman IS, Murphy DL. Neurological and neuropsychological studies of patients with obsessive- compulsive disorder. Biol Psichiatry 1983;18:741-751.
Jenike MA, Brotman AW. The EEG in obsessive-compulsive disorder. J Clin Psychiatry 1984;45(3):122-124.
Rockwell FV, Simons DJ. The electroencephalogram and personality organization in the obsessive-compulsive reactions. Arch Neurol Psychiatry 1947; 57:71-80.
Perros P, Young ES, Ritson JJ, Price GW, Mann P. Power spectral EEG analysis and EEG variability in obsessive-compulsive disorder. Brain Topography 1992;4(3):187-192.
Marsch GR, McCall VW. Sleep disturbances in psychiatric disease. En: Ebersole JS (ed.). Ambulatory EEG monitoring. New York: Raven Press; 1989.
Livanov MN. Information processing in the nervous system. Trabajo presentado en el XXII Congreso Internacional de Ciencias Fisiológicas, Leiden. Amsterdam: Excerpta Medica Foundation; 1962; p. 899.
Aslanov AS. On various features of the spatial distribution of biopotentials in the cerebral cortex of patients with an obsessive neurosis. Zh Nevropatol Psikhiatr Im S S Korsakova 1968;68(7):1019-1026.
Ricardo-Garcell J. Aportes del electroencefalograma convencional y el análisis de frecuencias para el estudio del Trastorno por Déficit de Atención. Primera parte. Salud Mental 2004;27(1):22-27.
Ricardo-Garcell J, Galindo y Villa G. El Trastorno por Déficit de Atención: un enfoque multidisciplinario. Revista Latina de Pensamiento y Lenguaje, número monográfico («Electrofisiología y Cognición») 2004;6(2B):247-270.
Matousek M, Petersen I. Frequency analysis of the EEG in normal children and adolescents. En: Kellaway P, Petersen I (eds.). Automatic assessment of the EEG. New York: Raven Press; 1973.
John ER, Ahn H, Prichep L, Trepetin M, Brown D et al. Developmental equations for the EEG. Science 1980;210:1255-1258.
Harmony T, Marosi E, Díaz De León AE, Becker J, Fernández T. Effect of sex, psychosocial disadvantages and biological risk factors on EEG maturation. Electroenceph Clin Neurophysiol 1990;75:482-491.
Harmony T, Fernández-Bouzas A. Mapeo del EEG en el estudio de los pacientes con lesiones expansivas intracraneales. Archivos Clínica Neurológica Querétaro 1995;4:20-24.
Bucci P, Mucci A, Volpe U, Merlotti E, Galderisi S et al. Executive hypercontrol in obsessive-compulsive disorder: electrophysiological and neuropsychological indices. Clin Neurophysiol 2004;115(6):1340-1348.
Khanna S. Obsessive-Compulsive disorder: is there a frontal lobe dysfunction? Biol Psychiatry 1988;24:602-613.
Molina V, Montz R, Pérez-Castejon MJ, Martin-Loeches M, Carreras JL et al. Cerebral perfusion, electrical activity, and effects of serotoninergic treatment in obsessive-compulsive disorder. Neuropsychobiology 1995;32:139-148.
Karadag F, Oguzhanoglu NK, Kurt T, Oguzhanoglu A, Atesci F et al. Quantitative EEG analysis in obsessive compulsive disorder. Int J Neurosci 2003;113(6):833-847.
Pogarell O, Juckel G, Mavrogiorgou P, Mulert C, Folkerts M et al. Symptom-specific EEG power correlations in patients with obsessivecompulsive disorder. Int J Psychophysiol 2006;62(1):87-92.
Simpson HB, Tenke CE, Towey JB, Liebowitz MR, Bruder GE. Symptom provocation alters behavioral ratings and brain electrical activity in obsessive- compulsive disorder: a preliminary study. Psychiatry Res 2000;95(2):149-155.
Hansen ES, Prichep LS, Bolwing TG, John ER. Quantitative electroencephalography in OCD patients treated with paroxetine. Clin Electroencephalogr 2003;34(2):70-74.
Fernández-Bouzas A, Harmony T, Fernández T, Aubert E, Ricardo-Garcell J et al. Sources of abnormal EEG activity in spontaneous intracerebral hemorrhage. Clin Electroencephalogr 2002;33(2):70-76.
Pascual-Marqui RD. LORETA in 3d solution space. Newsletter 1995;6:22-24.
Pascual-Marqui RD, Michel CM, Lehman D: Low resolution electromagnetic tomography: a new method for localizing electrical activity in the brain. Int J Psychophysiol 1994;18:49-65.
Bosch-Bayard J, Valdés-Sosa P, Virués-Alba T, Aubert-Vázquez E, John ER et al. 3D statistical parametric mapping of EEG source spectra by means of variable resolution electromagnetic tomography (VARETA). Clin Electroencephalogr 2001;32(2):47-61.
Fernández-Bouzas A. El mapeo del electroencefalograma cuantificado en el estudio de diversas entidades patológicas intracraneales. Su relación con la tomografía computada. Tesis doctoral en Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla, Querétaro; 1999.
Valdés-Sosa P, García F, Casanova R. Variable resolution electromagnetic tomography. En: Wood C (ed.). Proceedings of the 10th International Conference on Biomagnetism. Santa Fe, New Mexico: BIOMAG; 1996.
Sherlin L, Congedo M. Obsessive-compulsive dimension localized using low-resolution brain electromagnetic tomography (LORETA). Neurosci Lett 2005;387(2):72-74.
Bolwig TG, Hansen ES, Hansen A, Merkin H, Prichep LS. Toward a better understanding of the pathophysiology of OCD SSRI responders: QEEG source localization. Acta Psychiatr Scand 2007;115(3):237-42.
Hughes JR, John ER. Conventional and quantitative electroencephalography in psychiatry. J Neuropsychiatry Clin Neurosci 1999;11(2):190-208.
John ER, Prichep LS, Fridman J, Easton P. Neurometrics: computer-assisted differential diagnosis of brain dysfunctions. Science 1988;239(4836):162-169.
Rugg MD, Coles MGH (eds.). Electrophysiology of mind: Event-related brain potentials and cognition. USA: Oxford University Press; 1996.
Lopes da Silva F. Event-related potentials: methodology and quantification. En: Niedermeyer E, Lopes da Silva F (eds.). Electroencephalography, basic principles, clinical applications, and related fields. Philadelphia: Williams & Wilkins; 2005.
Polich J, Criado JR. Neuropsychology and neuropharmacology of P3a and P3b. Int J Psychophysiol 2006;60(2):172-185.
Daffner KR, Mesulam MM, Scinto LF, Calvo V, Faust R et al. An electrophysiological index of stimulus unfamiliarity. Psychophysiology 2000;37(6):737-747.
Patel SH, Azzam PN. Characterization of N200 and P300: selected studies of the event-related potential. International J Medical Science 2005;2(4):147-154.
Ciesielski KT, Beech HR, Gordon PK. Some electrophysiological observations in obsessional states. Br J Psychiatry 1981;138:479-484.
Towey JP, Bruder GEM, Hollander E, Friedman D, Erhan H et al. Endogenous event-related potentials in obsessive-compulsive disorder. Biol Psychiatry 1990;28:92-98.
Papageorgiou C, Rabavilas A, Liaappas I. Do obsessive-compulsive patients and abstinent heroin addicts share a common psychophysiological mechanism? Neuropsychobiology 2003;47:1-11.
Di Russo F, Zaccara G, Ragazzoni A, Pallanti S. Abnormal visual eventrelated potentials in obsessive-compulsive disorder without panic disorder or depression comorbidity. J Psychiatr Res 2000;34:73-82.
Johannes S, Wieringa BM, Nager W, Rada D, Müller-Vahl K et al. Tourett syndrome and obsessive-compulsive disorder: event-related brain potentials show similar mechanisms of frontal inhibition but dissimilar target evaluation processes. Behav Neurol 2003;14:9-17.
Towey JP, Bruder GE, Tenke CE, Leite P, Decaria C et al. Event-related potential and clinical correlates of neurodysfunction in obsessive-compulsive disorder. Psychiatry Res 1993;49:167-181.
Morault P, Guillem F, Bourgeois M, Laville J, Bensch C et al. Psychophysiological and clinical value of event-related potentials in obsessivecompulsive disorder. Biol Psychiatry 1997;42:46-56.
Morault P, Guillem F, Bourgeois M, Paty J. Improvement predictors in obsessive-compulsive disorder. An event-related potential study. Psychiatry Res 1998;81:87-96.
De Groot CM, Torello MW, Boutros NN, Allen R. Auditory event-related potentials and statistical probability mapping in obsessive-compulsive disorder. Clin Electroencephalogr 1997;28(3):148-154.
Hajcak G, Simons RF. Error-related brain activity in obsessive-compulsive disorder undergraduates. Psychiatry Res 2002;110:63-72.
Ruchsow M, Grön G, Reuter K, Spitzer M, Hermle L et al. Error-related brain activity in patients with obsessive-compulsive disorder and healthy controls. J Psychophysiology 2005;19(4):298-304.
Nieuwenhuis S, Nielen MM, Mol N, Hajcak G, Veltman DJ. Performance monitoring in obsessive-compulsive disorder. Psychiatry Res 2005;134:11-122.
Hajcak G, Franklin ME, Foa EB, Simons RF. Increased error-related brain activity in pediatric obsessive-compulsive disorder before and after treatment. Am J Psychiatry 2008;165(1):116-23.