Location of Repository

Abnormal P300 in people with high risk of developing psychosis

By Elvira Bramon, Madiha Shaikh, Matthew R. Broome, Julia Lappin, Daniel Bergé, Fern Day, J. B. (James B.) Woolley, Paul Tabraham, Mercè Madre, Louise C. Johns, Lucia Valmaggia, Victor Pérez, Pak Sham, MRC Psych MRCP M Phil MD Robin Murray and Philip McGuire


Background\ud \ud Individuals with an “at-risk mental state” (or “prodromal” symptoms) have a 20–40% chance of developing psychosis; however it is difficult to predict which of them will become ill on the basis of their clinical symptoms alone. We examined whether neurophysiological markers could help to identify those who are particularly vulnerable.\ud Method\ud \ud 35 cases meeting PACE criteria for the at-risk mental state (ARMS) and 57 controls performed an auditory oddball task whilst their electroencephalogram was recorded. The latency and amplitude of the P300 and N100 waves were compared between groups using linear regression.\ud Results\ud \ud The P300 amplitude was significantly reduced in the ARMS group [8.6 ± 6.4 microvolt] compared to controls [12.7 ± 5.8 microvolt] (p < 0.01). There were no group differences in P300 latency or in the amplitude and latency of the N100. Of the at-risk subjects that were followed up, seven (21%) developed psychosis.\ud Conclusion\ud \ud Reduction in the amplitude of the P300 is associated with an increased vulnerability to psychosis. Neurophysiological and other biological markers may be of use to predict clinical outcomes in populations at high risk

Topics: RC0321, BF
Publisher: Elsevier
OAI identifier: oai:wrap.warwick.ac.uk:100

Suggested articles



  1. (2006). A multivariate electrophysiological endophenotype, from a unitary cohort, shows greater research utility than any single feature in the Western Australian family study of schizophrenia. doi
  2. (2006). A Ser9Gly polymorphism in the dopamine D3 receptor gene (DRD3) and event-related P300 potentials. doi
  3. (1986). A Solution for Reliable and Valid Reduction of Ocular Artifacts, Applied to the P300 Erp. doi
  4. (2000). Alteration of event related potentials in siblings discordant for schizophrenia. doi
  5. (1983). Altered P300 topography in schizophrenia. doi
  6. (1997). Amplitude reductions and latency delays of the N100 wave have been described in chronic schizophrenia (Frangou
  7. (2007). Application of electroencephalography to the study of cognitive and brain functions in schizophrenia. doi
  8. (1983). As for the topography, the P300 amplitude deficits in the at-risk cases were consistently observed in midline as well as temporal sites (McCarley et al., 1991; McCarley et al., 2002; Morstyn et al.,
  9. (2002). Association between smaller left posterior superior temporal gyrus volume on magnetic resonance imaging and smaller left temporal P300 amplitude in first-episode schizophrenia. doi
  10. (2006). Association study of COMT gene Val158Met polymorphism with auditory P300 and performance on neurocognitive tests in patients with schizophrenia and their relatives. doi
  11. (2005). Attention orienting dysfunction during salient novel stimulus processing in schizophrenia. doi
  12. (2004). Auditory and visual P300 amplitude reduction in patients with prodromal symptoms of schizophrenia.
  13. (1981). Auditory event related potentials in schizophrenia and depression. doi
  14. (2004). Auditory event-related potential abnormalities in bipolar disorder and schizophrenia. doi
  15. (1999). Auditory event-related potentials and clinical scores in unmedicated schizophrenic patients. doi
  16. (1991). Auditory P300 and Eye Tracking Dysfunction in Schizophrenic Pedigrees. doi
  17. (2005). Auditory P300 in high-risk, recent-onset and chronic schizophrenia. doi
  18. (2006). Auditory P300 latency prolongation with age in schizophrenia: gender and subcomponent effects. doi
  19. (2001). Button-pressing affects P300 amplitude and scalp topography. doi
  20. (2004). Causal association between cannabis and psychosis: examination of the evidence. doi
  21. (1984). Clinical applications of the P3 component of event-related potentials II. Dementia, depression and schizophrenia. doi
  22. (2007). Cognitive functioning in the schizophrenia prodrome. doi
  23. (2005). Cognitive-behavioral therapy in the pre-psychotic phase: an exploratory study. doi
  24. (2007). Deconstructing schizophrenia: an overview of the use of endophenotypes in order to understand a complex disorder. doi
  25. (2001). Diagnosing schizophrenia in the initial prodromal phase. doi
  26. (1994). Diagnostic interview for genetic studies. Rationale, unique features, and training.
  27. (2007). Differential clinical, structural and P300 parameters in schizophrenia patients resistant to conventional neuroleptics. Prog Neuropsychopharmacol Biol Psychiatry. doi
  28. (1999). Diminished responsiveness of ERPs in schizophrenic subjects to changes in auditory stimulation parameters: implications for theories of cortical dysfunction. doi
  29. (2006). Endophenotypes in the genetic analysis of mental disorders. doi
  30. (1994). ERPs in schizophrenia: effects of antipsychotic medication. doi
  31. (2006). Event-related potential correlates of depression, insight and negative symptoms in males with recentonset psychosis. doi
  32. (2001). Event-related potentials and genetic risk for schizophrenia. doi
  33. (2005). Event-related potentials elicited by distractors in an auditory oddball paradigm in schizophrenia. doi
  34. (1991). Event-related potentials in schizophrenia: their biological and clinical correlates and a new model of schizophrenic pathophysiology. doi
  35. (1980). Event-related potentials in schizophrenics. doi
  36. (2006). Event-related potentials to auditory and visual selective attention in schizophrenia. doi
  37. (2002). From twin studies we know that P300 traits are reliable and heritable (Hall et al., 2006a; Hall et al., 2006b; Hall et al., 2004; van Beijsterveldt
  38. (2006). Generalized and specific neurocognitive deficits in prodromal schizophrenia. doi
  39. (2007). Genetic overlap between bipolar illness and event-related potentials. Psychol Med, doi
  40. (2006). Genetic overlap between P300, P50, and duration mismatch negativity. doi
  41. (2005). Imaging frontostriatal function in ultra-high-risk, early, and chronic schizophrenia during executive processing. doi
  42. (2006). Increasing task difficulty and using multi-modal techniques (Bender et al., 2007; Molina et al., 2007; Price et al., 2006; Sponheim et al.,
  43. (2000). Information processing deficits in relatives of manic depressive patients. doi
  44. (2006). Inherited auditory-cortical dysfunction in twin pairs discordant for schizophrenia. doi
  45. (2005). Is the P300 wave an endophenotype for schizophrenia? A meta-analysis and a family study. doi
  46. (2005). Is the P300 wave an endophenotype for schizophrenia? A metaanalysis and a family study. doi
  47. (2006). Is there an association between the COMT gene and P300 endophenotypes? doi
  48. (2005). Mapping the onset of psychosis: the Comprehensive Assessment of At-Risk Mental States. doi
  49. (2005). Memory impairments identified in people at ultra-high risk for psychosis who later develop first-episode psychosis. doi
  50. (2004). Mismatch negativity in schizophrenia: a family study. doi
  51. (2007). N100 and P300 amplitude to Go and No-Go variants of the auditory oddball in siblings discordant for schizophrenia. Schizophr Res. doi
  52. (2006). Neural anomalies during sustained attention in first-degree biological relatives of schizophrenia patients. doi
  53. (2003). Neuroanatomical abnormalities before and after onset of psychosis: a cross-sectional and longitudinal MRI comparison. doi
  54. (2007). Neurocognitive deficits in the (putative) prodrome and first episode of psychosis. doi
  55. (2007). Neurocognitive indicators for a conversion to psychosis: Comparison of patients in a potentially initial prodromal state who did or did not convert to a psychosis. doi
  56. (2004). Neurocognitive risk factors identified in the New York recognition and prevention (RAP)
  57. (2007). Neurophysiological endophenotypes of schizophrenia: the viability of selected candidate measures. doi
  58. (2007). None of the co-authors has any conflict of interests to declare.Bramon, et al. 13
  59. (2004). Olanzapine for treatment of the schizophrenia prodrome: 2-year results of a randomized placebo-controlled study. doi
  60. (2005). our data and a previous smaller study
  61. (1999). Our findings are consistent with the data from two previous smaller studies of the P300 in the ARMS, both of which reported reductions in amplitude (Mathalon et al., 2004; van der Stelt et al.,
  62. (2005). Outreach and support in south London (OASIS): implementation of a clinical service for prodromal psychosis and the at risk mental state. doi
  63. (1989). P3 in schizophrenia is affected by stimulus modality, response requirements, medication status, and negative symptoms. doi
  64. (2003). P300 and genetic risk for schizophrenia. doi
  65. (2007). P300 asymmetry and positive symptom severity: a study in the early stage of a first episode of psychosis. doi
  66. (2005). P300 paradigm: The P300 and N100 were obtained with a standard auditory oddball paradigm
  67. (1999). P300 subcomponents reflect different aspects of psychopathology in schizophrenia. doi
  68. (2007). PACE: a specialised service for young people at risk of psychotic disorders. doi
  69. (2005). Pharmacological intervention in the initial prodromal phase of psychosis. doi
  70. (2005). Predicting schizophrenia: findings from the Edinburgh High-Risk Study. doi
  71. (2005). Prepsychotic phase of schizophrenia and related disorders: recent progress and future opportunities.
  72. (2007). Prolongation of P300 latency is associated with the duration of illness in male schizophrenia patients. doi
  73. (2006). Prospective investigations of the prodromal state of schizophrenia: review of studies. doi
  74. (2003). Psychosis prediction: 12-month follow up of a high-risk (&quot;prodromal&quot;) group. doi
  75. (2004). Qualitatively similar, but less severe, deviances in amplitude and latency are also evident in the non-psychotic relatives of patients with schizophrenia
  76. (2002). Randomised controlled trial of early detection and cognitive therapy for preventing transition to psychosis in high-risk individuals - Study design and interim analysis of transition rate and psychological risk factors. doi
  77. (2002). Randomized controlled trial of interventions designed to Bramon, et al. 16 reduce the risk of progression to first-episode psychosis in a clinical sample with subthreshold symptoms. doi
  78. (2003). Randomized trial of olanzapine versus placebo in the symptomatic acute treatment of the schizophrenic prodrome. doi
  79. (2007). Recruitment and treatment practices for help-seeking &quot;prodromal&quot; patients. doi
  80. (2007). Relationship of imprecise corollary discharge in schizophrenia to auditory hallucinations. doi
  81. (1958). Report to the committee on methods of clinical examination in electroencephalography. doi
  82. (2006). Risk and protection in prodromal schizophrenia: ethical implications for clinical practice and future research. doi
  83. (2004). Risk factors for psychosis in an ultra high-risk group: psychopathology and clinical features. doi
  84. (2004). Risk factors for transition to first episode psychosis among individuals with 'at-risk mental states'. doi
  85. (2000). Schizophrenia-like deficits in auditory P1 and N1 refractoriness induced by the psychomimetic agent phencyclidine (PCP). doi
  86. (2004). Sensory gating deficits during the midlatency phase of information processing in medicated schizophrenia patients. doi
  87. (1969). Statistical Power Analysis for the Behavioral Sciences, doi
  88. (2007). Substantial Shared Genetic Influences on Schizophrenia and Event-Related Potentials. doi
  89. (2002). Target and non-target ERP disturbances in first episode vs. chronic schizophrenia. Clin Neurophysiol 113, 1754-1763.Bramon, et doi
  90. (2004). Test-retest reliability of ERP components of P300, P50 and duration mismatch negativity in monozygotic twins. doi
  91. (2003). The endophenotype concept in psychiatry: Etymology and strategic intentions. doi
  92. (2007). The initial prodrome of schizophrenia: different duration, different underlying deficits? doi
  93. (1997). The Maudsley family study .2. Endogenous event-related potentials in familial schizophrenia. doi
  94. (2004). The NoGo P300 'anteriorization' effect and response inhibition. doi
  95. (2003). The PRIME North America randomized double-blind clinical trial of olanzapine versus placebo in patients at risk of being prodromally symptomatic for psychosis. II. Baseline characteristics of the &quot;prodromal&quot; sample. doi
  96. (2000). Trait and state aspects of P300 amplitude reduction in schizophrenia: a retrospective longitudinal study. doi
  97. (2005). Transition to psychosis was defined using the threshold criteria in the CAARMS (Yung et al.,
  98. (2001). Treatment of the schizophrenia prodrome: is it presently ethical? doi
  99. (2002). Twin and family studies of the human electroencephalogram: a review and a meta-analysis. doi
  100. (2005). we failed to find latency deficits in the ARMS group. Because individuals at increased genetic risk of schizophrenia consistently show moderate latency delays (Bramon et al.,
  101. (2005). What causes the onset of psychosis? doi
  102. (2007). Which perspectives can endophenotypes and biological markers offer in the early recognition of schizophrenia? doi
  103. (2007). While ageing and task difficulty are known to influence P300 performance, especially its latency

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.