- Email: [email protected]
The effects of distracter stimuli upon saccade latency in schizophrenics
Abstracts
252. PREDICTIVE AND VISUALLY-GUIDED SACCADES IN OBSESSIVE-COMPULSIVE DISORDER R.H. Farber', B.A. Clementz.', M.N. Lam", & N.R. Swerdlow' 'Department of Psychology. University of Catifomi:l. San Diego. San Diego. CA 92093·0109; ;lDepartment of Psychology. University of Nebraska, Lincoln; ~Dcpartment of Psychiatry, University of Callfornia, San Diego Two independent studies were conducted 10 evaluate ocular motor performance of obsessive compulsive disorder (OeD) patients during predictive and visually-guided saccade tasks. For Study I. }2 OCD and 12 nonpsychlatric subjects were admlnistered three variations of a predictive saccadic tracking task: (1) a regular condition in which the current stimulus was extinguished contemporaneous with the illumination of the new target: (2) a gap condition in which the current stimulus was extinguished 250 llISCC prior to the illumination of the new target; and (3) an overlap condition in which blue. target-sized dots were continuously present lit the to-be- illuminated target locations. OCD and nonpsychiatrie subjects were able to decrease saccadic reaction times across trials suggesting that both groups developed u predictive strategy, In the gap condition. however, OCD patients decreased their reaction times at a slower rate than nonpsychlatric subjects. OCD patients also generated smaller amplitude saccades relative to nonpsychlatric subjects. Study 2 was undertaken in an effort to replicate and extend these findings. An additional 12 OCD lind 12 nonpsychiatrie subjects were administered both vlsumly-gulded lind predictive saccade tasks, OeD and nonpsychiatrie subjects did not differ on any aspect of visuallyguided saccade performance, Consistent with Study 1. both groups were able to decrease snccadic reaction times across trials during predictive tracking, Across predictive conditions, OCD patients again generated significantly smaller amplitUde saccades relative to ncnpsychiatrlc subjects. The Study I Ilnd Study 2 results will be discussed with respect to basal ganglla-thalnmoconkal pathology in oeD.
253. THE EFFECTS OF DISTRACTER STIMULI UPON SACCADE LATENCY IN SCHIZOPHRENICS B.D. Schwarta'r', W. 1. Evans l •2 •3 , B. O'Brienv'', M. Fogarty', & D.K. Winstead l •2 "Tulane University School of Medicine, Department of Psychiatry and Neurology; ~Veteruns Admtnistration Medical Center; 3Tulane Univeri>ity. Department of Psychology Infonnation processing dcflcitsare conslstently observed in schlzophrenics and include abnormalities of smooth pursuit eye movements. saccadic eye movements and uttentlon, Research reveals thatat leastsomeof these deficits may share u common neurophysiologic substrate. For instance. the processes involved in the movement of attention (dlscngnge, move, and re-engage) arc thought to precede and parallel saccadic eye movements. Furthermore. saccade latency can be speeded or delayed by manipulaung auentional demands. In the "Gap" condltion, saccade
DlOL PSYCUIATRY
1996;39:500-666
573
latency is reduced by offsetting a central fixation point prior to a target onset. The latency reduction results from the prior disengagement of attention. Saccade latency is prolonged when a contralateral distrncter stimulus is presented simultaneous withthe targetstimulus. Theeffect is thought to result from the time necessary to inhibit response to the distracter. The present studyassessed saccadic eye movement latency in schizophrenia using Gap and Distrncter conditions. Preliminary results reveal that schizophrenics produce slower saccades than normals in the single target Gap condition and that saccade latency docs not differ between the twogroups in the presence of distracter stimuli. However. in the Dlstmcter condition. both groups produce a significant number of incorrect saccades to the distracter stimuli. An analysts of these error latencies and the latency for the corrective saccade to the target reveals the following: I) Schizophrenics generate fasterlatency errorsaccades to the right visual fleld than to the left while normals do not show lin asymmetry: and 2) Schizophrenics require a longerlatency than normals to produce II correeuve saccades to the target. These results will be discussed in tenus of the neurophysiologic mechanisms thatsignal target onsetsand regulate attentional processes.
254. NEURAL SUBSTRATES OF EYE
TRACKING DEFICITS IN RELATIVES OF SCHIZOPHRENICS
G.A. O'DriSC'oU I •2 .3 , C. Benkelfat2 •3 ,4, R. Joober', S. LaI 2 •3 , & A,C.Evans4 'McGill University, Dept, of Psychology, Montreal. Quebec Canada H3A III I; ~Douglas Hospital Schizophrenia Research Center, Verdun, QC; 3McGill University Dept. of Psychiatry, Montreal, QC; 4Montreal Neurological Institute. McConnell Bruin Imaging Unit. Montreal, QC Compared with normal controls, schizophrenic patients and their first degree relatives have elevated rates of abnormal eye tracking. This familial pattern is not found in non-schizophrenic psychotic disorders. These data suggest that eye tracking deflcits are a manifestation of a genetically mediated brain pathology in schizophrenia. We used positron emission tomography (PET) and the I~O waterbolussubtraction method to characterize differences in regional brainfunction between Iirst-degrce . retatlves and matched controls during threeeye movement tasks, smooth pursuit. saccadcs and fixation. We compared averaged maps of relative blood now changes to assess differences in activntion during smooth pursuit compared with fixation between groups. Eye movements were monitored in the PETcamera withhigh-speed infrared oculography. We predicted that relatives lind controls would differ in actlvation of frontal eyefields. a hypothesis supported by correlations between pursuit quality and performance on frontal neuropsychological tasks in schizophrenic patients and relatives (Kntsnnis and Iacono 1991; Park and Holzman 1994). Preliminary results (5 controls. 5 first degree relatives) do not support this prediction, During pursuit. relatives had significantly lower blood now than controls in two areas important to pursuit, visual association cortex (t=5.7) and the human homologue of motion area MTIMST (l=3.9). Relatives hat! Increased blood now compared with controls in lenticular nuclei (t=6.3) and insula (t=4.5), two brain areas known to increase activation during saccades, Differences were also found in frontal cortex, where relatives had decreased activation in mea 11 (t""4.1) and lncrcascd activation in area 47 (l-S.9). Research supported by NARSAD and the Scottish Rite Schlzopbrenia Research Program.
252. PREDICTIVE AND VISUALLY-GUIDED SACCADES IN OBSESSIVE-COMPULSIVE DISORDER R.H. Farber', B.A. Clementz.', M.N. Lam", & N.R. Swerdlow' 'Department of Psychology. University of Catifomi:l. San Diego. San Diego. CA 92093·0109; ;lDepartment of Psychology. University of Nebraska, Lincoln; ~Dcpartment of Psychiatry, University of Callfornia, San Diego Two independent studies were conducted 10 evaluate ocular motor performance of obsessive compulsive disorder (OeD) patients during predictive and visually-guided saccade tasks. For Study I. }2 OCD and 12 nonpsychlatric subjects were admlnistered three variations of a predictive saccadic tracking task: (1) a regular condition in which the current stimulus was extinguished contemporaneous with the illumination of the new target: (2) a gap condition in which the current stimulus was extinguished 250 llISCC prior to the illumination of the new target; and (3) an overlap condition in which blue. target-sized dots were continuously present lit the to-be- illuminated target locations. OCD and nonpsychiatrie subjects were able to decrease saccadic reaction times across trials suggesting that both groups developed u predictive strategy, In the gap condition. however, OCD patients decreased their reaction times at a slower rate than nonpsychlatric subjects. OCD patients also generated smaller amplitude saccades relative to nonpsychlatric subjects. Study 2 was undertaken in an effort to replicate and extend these findings. An additional 12 OCD lind 12 nonpsychiatrie subjects were administered both vlsumly-gulded lind predictive saccade tasks, OeD and nonpsychiatrie subjects did not differ on any aspect of visuallyguided saccade performance, Consistent with Study 1. both groups were able to decrease snccadic reaction times across trials during predictive tracking, Across predictive conditions, OCD patients again generated significantly smaller amplitUde saccades relative to ncnpsychiatrlc subjects. The Study I Ilnd Study 2 results will be discussed with respect to basal ganglla-thalnmoconkal pathology in oeD.
253. THE EFFECTS OF DISTRACTER STIMULI UPON SACCADE LATENCY IN SCHIZOPHRENICS B.D. Schwarta'r', W. 1. Evans l •2 •3 , B. O'Brienv'', M. Fogarty', & D.K. Winstead l •2 "Tulane University School of Medicine, Department of Psychiatry and Neurology; ~Veteruns Admtnistration Medical Center; 3Tulane Univeri>ity. Department of Psychology Infonnation processing dcflcitsare conslstently observed in schlzophrenics and include abnormalities of smooth pursuit eye movements. saccadic eye movements and uttentlon, Research reveals thatat leastsomeof these deficits may share u common neurophysiologic substrate. For instance. the processes involved in the movement of attention (dlscngnge, move, and re-engage) arc thought to precede and parallel saccadic eye movements. Furthermore. saccade latency can be speeded or delayed by manipulaung auentional demands. In the "Gap" condltion, saccade
DlOL PSYCUIATRY
1996;39:500-666
573
latency is reduced by offsetting a central fixation point prior to a target onset. The latency reduction results from the prior disengagement of attention. Saccade latency is prolonged when a contralateral distrncter stimulus is presented simultaneous withthe targetstimulus. Theeffect is thought to result from the time necessary to inhibit response to the distracter. The present studyassessed saccadic eye movement latency in schizophrenia using Gap and Distrncter conditions. Preliminary results reveal that schizophrenics produce slower saccades than normals in the single target Gap condition and that saccade latency docs not differ between the twogroups in the presence of distracter stimuli. However. in the Dlstmcter condition. both groups produce a significant number of incorrect saccades to the distracter stimuli. An analysts of these error latencies and the latency for the corrective saccade to the target reveals the following: I) Schizophrenics generate fasterlatency errorsaccades to the right visual fleld than to the left while normals do not show lin asymmetry: and 2) Schizophrenics require a longerlatency than normals to produce II correeuve saccades to the target. These results will be discussed in tenus of the neurophysiologic mechanisms thatsignal target onsetsand regulate attentional processes.
254. NEURAL SUBSTRATES OF EYE
TRACKING DEFICITS IN RELATIVES OF SCHIZOPHRENICS
G.A. O'DriSC'oU I •2 .3 , C. Benkelfat2 •3 ,4, R. Joober', S. LaI 2 •3 , & A,C.Evans4 'McGill University, Dept, of Psychology, Montreal. Quebec Canada H3A III I; ~Douglas Hospital Schizophrenia Research Center, Verdun, QC; 3McGill University Dept. of Psychiatry, Montreal, QC; 4Montreal Neurological Institute. McConnell Bruin Imaging Unit. Montreal, QC Compared with normal controls, schizophrenic patients and their first degree relatives have elevated rates of abnormal eye tracking. This familial pattern is not found in non-schizophrenic psychotic disorders. These data suggest that eye tracking deflcits are a manifestation of a genetically mediated brain pathology in schizophrenia. We used positron emission tomography (PET) and the I~O waterbolussubtraction method to characterize differences in regional brainfunction between Iirst-degrce . retatlves and matched controls during threeeye movement tasks, smooth pursuit. saccadcs and fixation. We compared averaged maps of relative blood now changes to assess differences in activntion during smooth pursuit compared with fixation between groups. Eye movements were monitored in the PETcamera withhigh-speed infrared oculography. We predicted that relatives lind controls would differ in actlvation of frontal eyefields. a hypothesis supported by correlations between pursuit quality and performance on frontal neuropsychological tasks in schizophrenic patients and relatives (Kntsnnis and Iacono 1991; Park and Holzman 1994). Preliminary results (5 controls. 5 first degree relatives) do not support this prediction, During pursuit. relatives had significantly lower blood now than controls in two areas important to pursuit, visual association cortex (t=5.7) and the human homologue of motion area MTIMST (l=3.9). Relatives hat! Increased blood now compared with controls in lenticular nuclei (t=6.3) and insula (t=4.5), two brain areas known to increase activation during saccades, Differences were also found in frontal cortex, where relatives had decreased activation in mea 11 (t""4.1) and lncrcascd activation in area 47 (l-S.9). Research supported by NARSAD and the Scottish Rite Schlzopbrenia Research Program.