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J Neurol Neurosurg Psychiatry 1999;67:497–503
EVect of interstimulus interval on visual P300 inParkinson’s disease Lihong Wang, Yoshiyuki Kuroiwa, Toshiaki Kamitani, Tatsuya Takahashi, Yume Suzuki,Osamu Hasegawa Abstract
assessments, as they might be influenced by Objective—Visual event related potentials
parkinsonian motor deficits during the task.
(ERPs) were studied during an oddball
P300 latency, which is presumed to indicate paradigm, to testify whether cognitive
the time required for task evaluation independ- slowing in Parkinson’s disease exists and
ent of motor processing,6 may be useful in to investigate whether cognitive infor-
mation processing can be influenced by
disease. There are some reports which provide diVerent interstimulus intervals (ISIs) of
evidence of cognitive slowing during auditory an oddball task in patients with Parkin-
or visual oddball tasks by showing delayed son’s disease and normal subjects.
P300 in Parkinson’s disease.7–11 However, there Methods—ERPs and reaction time were
are also reports showing normal P300 latency measured in 38 non-demented patients
with Parkinson’s disease and 24 healthy
P300 is usually evoked by an oddball task elderly subjects. A visual oddball para-
with an interstimulus interval (ISI) of 1000 ms digm was employed to evoke ERPs, at
to 2000 ms. The load on cognitive processing three diVerent interstimulus (ISI) inter-
systems varies with the rate at which infor- vals: ISI(S), 1600 ms; ISI(M), 3100 ms; and
mation is presented—that is, with the duration ISI(L), 5100 ms. The eVect of ISIs on ERPs
of the ISIs. A too fast or too slow stimulus and reaction time was investigated.
presentation sometimes may make the task dif- Results—Compared with the normal sub-
ficult to follow and to perform. Cognitive slow- jects, P300 latency at Cz and Pz was
ing in Parkinson’s disease is presumed to be significantly delayed after rare target
found only in tasks that place greater demands stimuli in patients with Parkinson’s dis-
on the subject’s cognitive capacity.16 Therefore, ease only at ISI(L). Reaction time was
we presumed that diVerent rates of information prolonged in patients at all the three ISIs,
presentation due to diVerent ISIs of an oddball compared
controls.
task may change the diYculty of the task, and There was also significantly delayed N200
and reduced P300 amplitude at Cz and/or
Parkinson’s disease. There have been few stud- Pz to rare non-target stimuli in patients at
ies on the influences of diVerent presentation the three ISIs, compared with the normal
rates on cognitive processing in patients with controls. During rare target visual stimu-
Parkinson’s disease and normal subjects.
lation, P300 latency and reaction time in
In this study, we intended to investigate the patients with Parkinson’s disease and
whether the changes of visual event related reaction time in the normal subjects were
potentials occur during rare target and rare gradually prolonged as the ISI increased.
non-target stimulation when diVerent ISIs are Department of
Conclusion—Prolonged N200 latency to
used. To testify whether cognitive slowing in Neurology, Yokohama
rare non-target stimuli might indicate
City University School
whether cognitive information processing can that automatic cognitive processing was
of Medicine, 3–9
be influenced by diVerent ISIs in patients with Fukuura,
slowed in Parkinson’s disease. Cognitive
Parkinson’s disease and normal subjects, visual Kanazawa-ku,
processing reflected by P300 latency to
ERPs and reaction time were measured during Yokohama, 236–0004,
rare target stimuli was influenced by
a modified oddball paradigm at short, medium, longer ISI in patients with Parkinson’s
and long interstimulus intervals: ISI(S), 1600 disease.
ms; ISI(M),3100 ms; and ISI(L), 5100 ms.
(J Neurol Neurosurg Psychiatry 1999;67:497–503)
Keywords: P300; interstimulus interval; oddball para- The subjects were 38 patients (14 men, 24 It has been a long debated question whether or women) with the definite clinical diagnosis of not there exists cognitive slowing in Parkin- idiopathic Parkinson’s disease and 24 elderly Yokohama City UniversitySchool of Medicine, 3–9 son’s disease.1–5 The neuropsychological tests healthy volunteers (11 men, 13 women). The employed to evaluate cognitive slowing are age of the Parkinson’s disease group ranged extremely varied. Until now, no consistent from 41 to 77 years, with a mean (SD) of 65.8 Telephone 0081 45 7872800; fax 0081 45 788 6041.
conclusion has been reached on the existence (8.8) years. The age of the normal control and nature of the cognitive slowing in Parkin- group ranged from 42 to 79 years, with a mean son’s disease. It is sometimes diYcult to evalu- (SD) of 65.2 (10.3) years. All control subjects ate mental processing in patients with Parkin- showed normal neurological findings and had son’s disease accurately by neuropsychological no specific neurological diseases. None exhib- Backgrounds of patients with Parkinson’s disease contained 12 to 16 responses to rare targetstimuli. Each section was repeated once to confirm the reliability of recording for each ISI.
The EEG activity was analysed 100 ms before and 900 ms after each visual presentation. On the traces, upward deflection of the ERP wave- nent (peak or notch) at Cz and Pz occurring 200–400 ms after the start of the stimulus.
P300 was identified as a positive wave at Cz and Pz, with latency of 300–700 ms after the start of the stimulus. N200 latency and P300 latency were measured as the interval between each peak (or notch) and the onset of the *The levodopa dosage in the table represents the dosage of stimulus. P300 amplitude was defined as the levodopa in Neodopaston® which contains levodopa and carbi- voltage diVerence between the P300 peak and the prestimulus baseline (averaging voltage of100 ms before the stimulus). Reaction time was ited any abnormal MRI findings. They also had defined as the interval between the start of rare no history of medical or psychiatric disorders.
All patients fulfilled Parkinson’s Disease Soci-ety Brain Bank clinical criteria17 for definitedisease. Patients with secondary parkinsonism or with evidence of focal cerebral lesions were A two tailed Student’s t test was used to com- excluded from the study. Any patients diag- pare the ERPs (N200 latency, P300 latency, nosed as having dementia according to the cri- and P300 amplitude) or reaction time between teria of the diagnostic and statistical manual of the Parkinson’s disease and normal groups at mental disorders, third edition, revised,18 were each of the three ISIs. One way repeated meas- excluded from the study. All patients were ures ANOVA was computed to study the effect of ISIs on ERPs (N200 latency, P300 latency, Table 1 shows the details of the patients with and P300 amplitude) or reaction time in the Parkinson’s disease. All the subjects gave Parkinson’s disease group and the normal con- signed informed consent after the purpose of trol group, separately. Two way repeated meas- the study and the protocol had been explained ures ANOVA was also studied using the groups (Parkinson’s disease v normal controls) as the between subjects factor and diVerent ISIs asthe within subjects factor. When ANOVAyielded significant diVerences among data sets, a Bonferroni/Dunn test was performed as a A modified visual oddball paradigm which was previously designed by Tachibana et al19 wasused to elicit ERPs (fig 1). The paradigmemployed three kinds of visual stimuli: rare tar-get, rare non-target, and frequent non-target.
They were presented on an electronic tachisto- All the normal subjects accurately performed scope screen (Iwasaki Tsushin), at event prob- the task. All patients with Parkinson’s disease abilities of 20%, 20%, and 60%, respectively.
performed the task at an error rate not exceed- The duration of each stimulus was 68 ms. The ISI was defined as the interval between the appearance of each sequential stimulus. The Parkinson’s disease (fig 2), P300 latency seems task was performed at short, medium, and long to be longer after rare target stimuli at ISI(L) ISI separately in the order of ISI(S) 1600 ms than at ISI(S) and ISI(M). P300 amplitude after rare non-target stimuli in patients with (stimulus rate 0.322 Hz), and ISI(L) 5100 ms Parkinson’s disease was markedly reduced (stimulus rate 0.196 Hz). The subjects were compared with that in normal controls at all instructed to press the button for rare target stimuli as rapidly and correctly as possible.
Data were recorded only after the subjectsunderstood the tasks completely through a trodes from Cz and Pz referred to linkedearlobes. The EOG was monitored using aforehead-temple montage with a rejection levelof ±100 µV. Electrode impedance was main- tained below 5 K . Bandwidth of preamplifiers ranged from 0.1 to 50 Hz. Each block included four rare target stimuli. Three or four blocks with breaks of 2 minutes between blocks com- Sketch representing the time course of the prised one section. Therefore, each section modified oddball paradigm at three diVerent ISIs. EVect of interstimulus on P300 in Parkinson’s disease Averaged waveforms of ERPs at Pz after rare target and rare non-target at ISI(S), ISI(M), and ISI(L) of the Parkinson’s disease (PD) and the normal control groups. no ISI eVect was found on any of ERP compo- BETWEEN PATIENTS WITH PARKINSON’S DISEASE nents after rare target and rare non-target stimuli. In the Parkinson’s disease group, only We compared the data between patients with P300 latency after rare target stimuli was found Parkinson’s disease and normal control groups to be significantly influenced by diVerent ISIs using Student’s t test (tables 2 and 3).
Prolonged P300 latency at Cz and Pz after rare Comparison of the mean (SD) values of ERPs at target stimuli in Parkinson’s disease was found Pz and reaction time (RT) to rare target stimuli betweenpatients with Parkinson’s disease (PD) and normal controls only at ISI(L) (Cz, t=2.408, df=52, p<0.05; Pz, t=2.232, df=52, p<0.05). No significant N200latency or P300 amplitude diVerence to rare target stimuli was found between groups at any of the three ISIs. Significantly delayed N200 at Parkinson’s disease was found at the three ISIs: ISI(S),(Pz, t=2.915, df=49, p<0.01); ISI(M), (Cz, t=2.269, df=50, p<0.05), and ISI(L),(Pz, t=2.871, df=45, p<0.01). Significantly reduced non-target stimuli was found in the Parkinson’s disease group compared with the control group at all the ISIs (ISI(S),Cz, t=2.741, df=58, t=2.530, df=56, p<0.05; ISI(L), Cz, t=2.508, *p<0.05; Student’s t test.
df=51, p<0.05; Pz, t=2.408, df=51, p<0.05).
Comparison of the mean (SD) values of ERPs at Reaction time to rare target stimuli in Parkin- Pz to rare non-target stimuli between patients with son’s disease was significantly delayed com- Parkinson’s disease (PD) and normal controls at the three pared with that in the control group at all the ISIs (ISI(S), t=2.098, df=51, p<0.05; ISI(M), t=2.475, df=49, p<0.05; ISI(L), t=2.483,df=48, p<0.05).
EFFECT OF ISI ON ERPS AND REACTION TIME IN ANOVA to study the eVect of the three ISIs on N200 and P300 components and reaction time in the Parkinson’s disease and the normal group, separately. In the normal control group, *p<0.05; **p<0.01; Student’s t test.
ISI eVect on reaction time in normal control group (open circles) and Parkinson’s disease group (closedcircles). S, M, and L indicate ISI(S), ISI(M), and ISI(L), respectively. The p value represents the eVect of ISIs on reaction time by one way repeated measures ANOVA. NS=no significant diVerence among three ISIs by one way stimuli (Cz, F=5.413, p<0.01; Pz, F=6.209, p<0.01). P300 latency at ISI(L) was signifi- cantly longer than at ISI(S) (Bonferroni/Dunn post hoc, Cz, p<0.05; Pz, p<0.05). However, ISI eVect on P300 latency at Cz and Pz in groups×ISIs did not influence P300 latency to normal control group(open circles) and Parkinson’s disease group (closed circles). S, M, and L indicate ISI(S), ISI(M) and ISI(L), respectively. The p value represents the groups made significant diVerences on N200 eVect of ISIs on P300 latency by one way repeated latency (Cz, F=7.415, p<0.01; Pz, F=9.595, measures ANOVA. NS=no significant diVerence among p<0.01) and P300 amplitude (Cz, F=8.905, three ISIs by one way repeated measures ANOVA. p<0.01; Pz, F=8.220, p<0.01) to rare non- F=8.094, p<0.001; Pz, F=5.006, p<0.05; fig 3 (Bonferroni/Dunn post hoc, Cz, p<0.01; Pz, significantly longer than at ISI(S) (Bonferroni/ Dunn post hoc, Cz, p<0.05; Pz, p<0.05). No (Bonferroni/Dunn post hoc, Cz, p<0.0001; Pz, ISI eVect was found on any other ERP compo- p<0.0001) to rare non-target stimuli compared nents after rare target and rare non-target with the control group. However, diVerent ISIs stimuli in the Parkinson’s disease group.
or the interaction of groups×ISIs made no sig- A significant ISI eVect on reaction time was nificant diVerence on N200 latency and P300 found in both the Parkinson’s disease group amplitude to rare non-target stimuli. DiVerent groups, diVerent ISIs, and the interaction of F=8.769, p<0.001; fig 4 and table 4) and the groups×ISIs influenced reaction time to rare normal control group (one way repeated meas- target stimuli significantly (diVerent groups, ures ANOVA, F=6.122, p<0.01). Reaction F=6.441, p<0.05; diVerent ISIs, F=12.069, time at ISI(L) was significantly longer than p<0.0001; groups × ISIs, F=3.339, p<0.05).
reaction time at ISI(S) (Bonferroni/Dunn post The patient group showed significantly more hoc, p<0.05) in the Parkinson’s disease group prolonged reaction time than the control group and tended to be longer than reaction time at (Bonferroni/Dunn post hoc, p<0.001). Reac- tion time at ISI(L) was significantly more pro- (Bonferroni/Dunn post hoc, p=0.0554).
(Bonferroni/Dunn post hoc, p<0.05). NeitherdiVerent groups nor diVerent ISIs had a THE EFFECTS OF GROUPS AND ISIS ON ERPS AND significant eVect on N200 latency and P300 REACTION TIMETwo way repeated measures ANOVA using the amplitude to rare target stimuli, or P300 diVerent groups (Parkinson’s disease v normal latency to rare non-target stimuli. Table 5 is a controls) as the between groups factor and the summary of the main significant findings in diVerent ISIs as the within subjects factor con- firmed that diVerent ISIs produced a signifi-cant P300 latency diVerence during rare target MEASUREMENT OF P300 LATENCY DIFFERENCE(RATIO) AND REACTION TIME DIFFERENCE(RATIO) IN PATIENTS WITH PARKINSON’S DISEASE Significant eVect of ISI on ERP and reaction time (RT) to rare target stimuli in patients withParkinson’s disease (PD) and normal controls during one As P300 latency and reaction time to rare tar- get stimuli were found to be influenced by dif-ferent ISIs, we measured P300 latency diVer- ence (or ratio) and reaction time diVerence (or ratio) for two diVerent ISIs. P300 latency Verences to rare target stimuli were defined as (P300 latency at ISI(M)−P300 latency at ISI(S)); (P300 latency at ISI(L)−P300 latency at ISI(M)); and (P300 latency at ISI(L)−P300 *p<0.05, **p<0.01; ***p<0.001.
latency at ISI(S)). reaction time diVerences EVect of interstimulus on P300 in Parkinson’s disease Significant group and/or ISI eVect on ERPs and RT found during two way elucidated why mean N200 latency in the Par-kinson’s disease group was delayed to rare non-targets and was not delayed to rare targets.
Literature on visual search (popout) shows that, even in normal subjects, verification of the presence of a target is completed more quickly than the decision that a target is absent.26 27 There is also a study showing that it was significantly worse at discerning the orientation of non-target regions than at detecting target presence.28 These results might be related to a self terminating processing theory that a visual *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001.
search can terminate on the half way when a predesignated target is found, while for a non- ISI(M)−reaction time at ISI(S)); (reaction target stimulus (a negative response), visual time at ISI(L)−reaction time at ISI(M)); and search must proceed until all features of the (reaction time at ISI(L)− reaction time at stimulus are evaluated.29 The significantly ISI(S)). P300 latency ratios to rare target delayed N200 to rare non-targets in our study might be a physiological correlate to the self ISI(M)/P300 latency at ISI(S)); (P300 latency terminating processing, albeit exaggerated in at ISI(L)/P300 latency at ISI(M)); and (P300 latency at ISI(L)/P300 latency at ISI(S)).
The controlled processing reflected by P300 Reaction time ratios were defined as (reaction latency after rare targets was slowed only at time at ISI(M)/reaction time at ISI(S)); (reac- longer ISI in Parkinson’s disease, but not at tion time at ISI(L)/reaction time at ISI(M)); and (reaction time at ISI(L)/reaction time at that there was no group diVerence on P300 ISI(S)). We compared the above parameters latency while taking all the three ISIs as a between groups by Student’s t test. Only P300 whole. This result is diVerent from the results of other authors who proved the cognitive ISI(L)−P300 latency at ISI(M)) at Cz and slowing during oddball task in Parkinson’s dis- P300 latency ratio of (P300 latency at ISI(L)/ ease by showing delayed P300 latency,9–11 but in P300 latency at ISI(M)) at Cz were signifi- cantly greater in patients with Parkinson’s dis- prolonged P300 latency in the disease.12–15 Dif- ease than those in normal controls (latency ferent clinical status such as age at test, age at diVerence, t=−2.098, p<0.05; latency ratio, onset, duration of illness, and treatment may be able to explain such discrepancy on P300latency.30 31 Although the interaction of groups×ISIs did Discussion
not influence P300 latency to rare target stimuli significantly after two way repeated reduced P300 amplitude at Cz and/or Pz to rare non-target stimuli at all the three ISIs, and that P300 latency to rare targets was signifi- prolonged P300 latency at Cz and Pz to rare cantly influenced by diVerent ISIs in the targets only at ISI(L). Visual N200 to rare tar- Parkinson’s disease group and not in the normal control group. Furthermore, Student’s auditory N2b20 and to be reflected an control- t test on P300 to rare targets showed that (P300 led discrimination processing.21 However, our visual N200 to rare non-target stimuli was ISI(L)−P300 latency at ISI(M)), and (P300 more similar to N2b described by Squires et al, latency at ISI(L)/P300 latency at ISI(M)) in which appeared while the subject was paying the Parkinson’s disease group showed signifi- unconscious attention and should reflect an cantly larger mean values than those in the automatic task evaluation processing.22 P300 normal control group. All these results sug- after rare non-target stimuli in our paradigm gested that the ISI eVect on P300 to rare was also thought to reflect an automatic task targets was rather stronger in the Parkinson’s evaluation processing,23 whereas P300 after disease group compared with the normal con- rare target stimuli could reflect controlled cog- trol group. Polich et al32 described significantly nitive processing.23 24 With regard to the longer auditory P300 latency at the ISI of 6 question whether cognitive slowing exists in seconds than the P300 latency at the ISI of 2 Parkinson’s disease or not, our finding of seconds in normal younger subjects. Literature prolonged N200 latency to rare non-targets about ISI eVects on P300 latency using visual implies that the automatic cognitive processing stimulation in Parkinson’s disease is completely could be slowed in the disease. Dysfunction of lacking. To our knowledge, this is the first automatic processing in Parkinson’s disease report that showed P300 changes at diVerent has also been reported by a recent ERP study.24 One possible explanation for delayed P300 studies25 which suggested preserved function of at ISI(L) is that it might be due to the decreas- automatic cognitive processing in parkinsonian ing sustained attention at longer ISI in Parkin- patients. Task diVerences while evaluating the son’s disease. It is said that sustained attention automatic cognitive processing may be a reason is impaired in Parkinson’s disease.33 34 In the longer ISI condition, the subjects had to try to some slowness of automatic cognitive process- maintain their attention for a relatively longer ing in Parkinson’s disease, whereas controlled period of time. Therefore, too slow information cognitive processing was slowed only at the input at ISI(L) might cause an eVort demand- ing task to patients with Parkinson’s disease.
latency and reaction time implied that the con- Further, to get the same number of trials per trolled cognitive processing in Parkinson’s dis- ISI condition, the total test session would be ease was influenced by slower information much longer in the longer ISI condition. Also, the ISI(L) task was always performed later thanISI(S) and ISI(M). All these facts could result We are grateful to Masaaki Sibuya, Professor of Statistics, Keio in low attention at longer ISI. However, if it University, Tokyo for helpful assistance and comments concern-ing statistical analysis. We also sincerely thank Ivan Bodis- were a problem of low attention at longer ISI, Wollner, Professor of Neurology and Ophthalmology, State University of New York, for valuable comments on the paper.
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