Access the full text.
Sign up today, get DeepDyve free for 14 days.
(2007)Norwegian Basic Aphasia Assessment
R. Näätänen (2001)The perception of speech sounds by the human brain as reflected by the mismatch negativity (MMN) and its magnetic equivalent (MMNm).
Psychophysiology, 38 1
R. Knight, D. Scabini, David Woods, C. Clayworth (1988)The effects of lesions of superior temporal gyrus and inferior parietal lobe on temporal and vertex components of the human AEP.
Electroencephalography and clinical neurophysiology, 70 6
G. Miceli, C. Caltagirone, G. Gainotti, P. Payer-Rigo (1978)Discrimination of voice versus place contrasts in aphasia
Brain and Language, 6
V. Csépe, Márk Molnár (1997)Towards the possible clinical application of the mismatch negativity component of event-related potentials.
Audiology & neuro-otology, 2 5
A. Rothenberger, zsef Szirtes, Reinhart Jtirgens (1982)Auditory evoked potentials to verbal stimuli in health, aphasic, and right hemisphere damaged subjects. Pathway effects and parallels to language processing and attention.
Archiv fur Psychiatrie und Nervenkrankheiten, 231 2
R. Knight, S. Hillyard, D. Woods, H. Neville (1980)The effects of frontal and temporal-parietal lesions on the auditory evoked potential in man.
Electroencephalography and clinical neurophysiology, 50 1-2
E. Renzi, P. Faglioni (1978)Normative Data and Screening Power of a Shortened Version of the Token Test
A. Thiel, K. Herholz, Adem Koyuncu, M. Ghaemi, L. Kracht, Birgit Habedank, W. Heiss (2001)Plasticity of language networks in patients with brain tumors: A positron emission tomography activation study
Annals of Neurology, 50
G. Yeni-Komshian, L. Lafontaine (1982)Discrimination and identification of voicing and place contrasts in aphasic patients.
Canadian journal of psychology, 37 1
G. Dorze, C. Brassard (1995)A description of the consequences of aphasia on aphasic persons and their relatives and friends, based on the WHO model of chronic diseases
J. Gandour, R. Dardarananda (1982)Voice onset time in aphasia: Thai. I. Perception
Brain and Language, 17
Colin Brown, P. Hagoort, T. Swaab (1996)Neurophysiological evidence for a temporal disorganization in aphasic patients with comprehension deficits
R. Näätänen, I. Winkler (1999)The concept of auditory stimulus representation in cognitive neuroscience.
Psychological bulletin, 125 6
T. Swaab, Colin Brown, P. Hagoort (1997)Spoken Sentence Comprehension in Aphasia: Event-related Potential Evidence for a Lexical Integration Deficit
Journal of Cognitive Neuroscience, 9
Martyn Hyde (1997)The N1 response and its applications.
Audiology & neuro-otology, 2 5
N. Varney (1984)Phonemic imperception in aphasia
Brain and Language, 21
Ray Johnson (2007)On the neural generators of the P300 component of the event-related potential.
Psychophysiology, 30 1
G. Miceli, G. Gainotti, C. Caltagirone, C. Masullo (1980)Some aspects of phonological impairment in aphasia
Brain and Language, 11
David Woods, Robert Knight, D. Scabini (1993)Anatomical substrates of auditory selective attention: behavioral and electrophysiological effects of posterior association cortex lesions.
Brain research. Cognitive brain research, 1 4
P. Praamstra, Dick Stegeman, Sabine Kooijman, J. Moleman (1993)Evoked potential measures of auditory cortical function and auditory comprehension in aphasia
Journal of the Neurological Sciences, 115
E. Sussman, T. Kujala, Jaana Halmetoja, H. Lyytinen, P. Alku, R. Näätänen (2004)Automatic and controlled processing of acoustic and phonetic contrasts
Hearing Research, 190
R. Näätänen (1992)Attention and brain function
A. Basso, G. Casati, L. Vignolo (1977)Phonemic Identification Defect in Aphasia
R. Knight, D. Scabini, D. Woods, C. Clayworth (1989)Contributions of temporal-parietal junction to the human auditory P3
Brain Research, 502
A. Rothenberger, J. Szirtes, R. Jürgens (1982)Auditory evoked potentials to verbal stimuli in healthy, aphasic, and right hemisphere damaged subjects
Archiv für Psychiatrie und Nervenkrankheiten, 231
P. Hagoort, Colin Brown, T. Swaab (1996)Lexical-semantic event-related potential effects in patients with left hemisphere lesions and aphasia, and patients with right hemisphere lesions without aphasia.
Brain : a journal of neurology, 119 ( Pt 2)
S. Blumstein, W. Cooper, E. Zurif, A. Caramazza (1977)The perception and production of Voice-Onset Time in aphasia
T. Jauhiainen, A. Nuutila (1977)Auditory perception of speech and speech sounds in recent and recovered cases of aphasia
Brain and Language, 4
P. Tallal, F. Newcombe (1978)Impairment of auditory perception and language comprehension in dysphasia
Brain and Language, 5
G. Hickok, D. Poeppel (2004)Dorsal and ventral streams: a framework for understanding aspects of the functional anatomy of language
Lutz Winhuisen, A. Thiel, B. Schumacher, J. Kessler, J. Rudolf, W. Haupt, W. Heiss (2005)Role of the Contralateral Inferior Frontal Gyrus in Recovery of Language Function in Poststroke Aphasia: A Combined Repetitive Transcranial Magnetic Stimulation and Positron Emission Tomography Study
Salvatore Giaquinto (2004)Evoked potentials in rehabilitation. A review.
Functional neurology, 19 4
T. Picton (1992)The P300 Wave of the Human Event‐Related Potential
Journal of Clinical Neurophysiology, 9
CM Brown, P Hagoort, TY Swaab (1997)Aphasietherapie im Wandel
Shari Baum (2002)Consonant and vowel discrimination by brain-damaged individuals: effects of phonological segmentation
Journal of Neurolinguistics, 15
(1982)Dardarananda R: Voice onset time in aphasia: Thai
E. Baker, S. Blumstein, H. Goodglass (1981)Interaction between phonological and semantic factors in auditory comprehension
Timothy Roberts, Paul Ferrari, Steven Stufflebeam, David Poeppel (2000)Latency of the auditory evoked neuromagnetic field components: stimulus dependence and insights toward perception.
Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society, 17 2
Wolf-Dieter Heiss, J. Kessler, Alexander Thiel, M. Ghaemi, H. Karbe (1999)Differential capacity of left and right hemispheric areas for compensation of poststroke aphasia
Annals of Neurology, 45
Pool Kd, T. Finitzo, Hong Ct, John Rogers, Pickett Rb (1989)Infarction of the superior temporal gyrus: a description of auditory evoked potential latency and amplitude topology.
Ear and hearing, 10 3
D. Caplan, D. Gow, N. Makris (1995)Analysis of lesions by MRI in stroke patients with acoustic‐phonetic processing deficits
R. Näätänen (2003)Mismatch negativity: clinical research and possible applications.
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 48 2
W. Milberg, S. Blumstein, B. Dworetzky (1988)Phonological processing and lexical access in aphasia
Brain and Language, 34
W. Pritchard, S. Shappell, M. Brandt (1991)Psychophysiology of N200/N400: A Review and Classification Scheme
R. Näätänen, T. Picton (1987)The N1 wave of the human electric and magnetic response to sound: a review and an analysis of the component structure.
Psychophysiology, 24 4
H. Semlitsch, P. Anderer, P. Schuster, O. Presslich (1986)A solution for reliable and valid reduction of ocular artifacts, applied to the P300 ERP.
Psychophysiology, 23 6
T. Swaab, Colin Brown, P. Hagoort (1998)Understanding ambiguous words in sentence contexts: electrophysiological evidence for delayed contextual selection in Broca’s aphasia
F. Becker, I. Reinvang (2007)Mismatch negativity elicited by tones and speech sounds: Changed topographical distribution in aphasia
Brain and Language, 100
I Reinvang (1985)Aphasia and Brain Organization
P. Square-Storer, F. Darley, R. Sommers (1988)Nonspeech and speech processing skills in patients with aphasia and apraxia of speech
Brain and Language, 33
S. Blumstein, E. Baker, H. Goodglass (1977)Phonological factors in auditory comprehension in aphasia
D. Linden (2005)The P300: Where in the Brain Is It Produced and What Does It Tell Us?
The Neuroscientist, 11
T. Ilvonen, T. Kujala, M. Tervaniemi, O. Salonen, R. Näätänen, R. Näätänen, E. Pekkonen, E. Pekkonen (2001)The processing of sound duration after left hemisphere stroke: event-related potential and behavioral evidence.
Psychophysiology, 38 4
Background: The role of impaired sound and speech sound processing for auditory language comprehension deficits in aphasia is unclear. No electrophysiological studies of attended speech sound processing in aphasia have been performed for stimuli that are discriminable even for patients with severe auditory comprehension deficits. Methods: Event-related brain potentials (ERPs) were used to study speech sound processing in a syllable detection task in aphasia. In an oddball paradigm, the participants had to detect the infrequent target syllable /ta:/ amongst the frequent standard syllable /ba:/. 10 subjects with moderate and 10 subjects with severe auditory comprehension impairment were compared to 11 healthy controls. Results: N1 amplitude was reduced indicating impaired primary stimulus analysis; N1 reduction was a predictor for auditory comprehension impairment. N2 attenuation suggests reduced attended stimulus classification and discrimination. However, all aphasic patients were able to discriminate the stimuli almost without errors, and processes related to the target identification (P3) were not significantly reduced. The aphasic subjects might have discriminated the stimuli by purely auditory differences, while the ERP results reveal a reduction of language-related processing which however did not prevent performing the task. Topographic differences between aphasic subgroups and controls indicate compensatory changes in activation. Conclusion: Stimulus processing in early time windows (N1, N2) is altered in aphasics with adverse consequences for auditory comprehension of complex language material, while allowing performance of simpler tasks (syllable detection). Compensational patterns of speech sound processing may be activated in syllable detection, but may not be functional in more complex tasks. The degree to which compensational processes can be activated probably varies depending on factors as lesion site, time after injury, and language task. Page 1 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 (reflected by N2a/MMN) which in turn trigger a target Background The analysis of speech sounds is a necessary step in the reaction . Cognitive processes related to target detec- process of language comprehension. Since most aphasic tion and to the engagement of a target reaction are patients have auditory comprehension deficits, the ques- reflected by the P3 component which is mainly generated tion whether and to what degree speech sound perception in parietal regions and in the case of auditory stimuli in is impaired in aphasia has been much investigated [1-15]. superior temporal cortex [24-26]. Several studies have indeed shown that aphasic subjects perform significantly worse than healthy controls in e.g. Electrophysiological studies of sub-lexical speech sound tasks where they have to decide whether two consonants processing in aphasia have mainly focused on unattended (or two syllables with different consonants) are the same phonetic/phonologic processing often using the mis- or not [1,3,4,8,9]. match negativity component (MMN; for a short overview of these studies, see ). To our knowledge, no ERP- However, most authors did not find correlations between investigations of attended processing of sub-lexical speech these speech perception impairments and auditory com- stimuli have been performed in aphasia. While the prehension abilities as measured by classical aphasia number of studies using simple language stimuli in assessments [2,4,7,11]. Rather, several studies have attended paradigms in order to investigate auditory revealed patients with severe auditory comprehension processing is small, more studies with non-speech stimuli deficits but no or minor speech sound perception impair- have been conducted, often using tones presented in odd- ments, or patients with mild auditory comprehension def- ball paradigms. There is good evidence for N1 amplitude icits who performed poorly in speech sound reduction to an attended and frequent tone stimulus in discrimination and identification tasks [2-4,6,9,15]. Thus, aphasia [28-32]. Regarding topographic distribution of a dissociation – at least partially – between speech percep- the N1 component, a right hemisphere maximum has tion and auditory comprehension has been found, which been observed in an aphasic group while a control group also has been quoted as evidence for a dual pathway showed an even hemispheric distribution . Lesions framework of language comprehension . However, a located in either left or right superior temporal gyrus were rather strong correlation between speech sound percep- found to be the cause for N1 amplitude reduction [33,34]. tion and auditory comprehension has also been reported When using monaural presentation in left hemisphere . injured patients, right-ear stimulation led to bilateral N1 reduction . Brain activity related to different stages of speech sound processing can be studied with event-related brain poten- Regarding the response to the target stimulus, reduced P3 tials. At about 100 ms after stimulus onset, a negativity amplitudes have been reported, especially in patients with can be recorded as the N1 wave which is generated in both severe comprehension deficits [29,31,36]. The temporo- temporal and frontal brain areas . N1 reflects an inter- parietal junction has been shown to be crucial for normal mediate stage in auditory analysis as well as sound detec- P3 amplitudes to tone stimuli . tion and orienting functions . Concerning the processing of speech sounds, N1 is suggested to reflect On the background of a still unclear relation between integrative processing of acoustic features of the incoming speech sound perception and auditory comprehension stream of speech, but not a neurological representation of and sparse ERP-research on the attended processing of phonemes [18-20]. speech sounds in aphasia, we aimed in this study to fur- ther explore neurophysiological correlates of automatic Also the N2 waveform – recorded at about 150 to 300 ms and cognitive processes involved in speech sound process- after stimulus onset – is a summation of several compo- ing in aphasic subjects. A major problem in interpreting nents . While early parts of the N2 (N2a or mismatch ERP-results and behavioral findings is that when the study negativity, MMN) reflect automatic deviance detection, person fails to perform the task correctly, it is impossible later stages of the N2 wave are regarded as correlates of to determine what underlying processes are active. Our attentional deviance detection (N2b) and of classification strategy is therefore to study ERP in a relevant linguistic processing (N2c). Starting with N2b and in further stages, task which can be performed adequately by aphasic sub- the processing of speech sounds seems to differ from that jects, and to investigate the relevance of deviations in of non-speech sounds, while sound processing is com- processing for the performance of a more complex task. mon for speech and non-speech in earlier stages as Having investigated automatic discrimination of syllables reflected by N2a . With regard to the time course of in an earlier study , we used the same stimuli in this attentional discrimination of stimuli, it is suggested that present study in an attended oddball design. A central the N2 component reflects processes of transient arousal research question was at which processing stages changes triggered by unattended discrimination processes may be found in aphasia. Current research is focusing on Page 2 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 changes of brain activation during recovery from brain both groups, most patients have lesions in the frontal injury, suggesting different activation patterns in patients and/or temporal lobes; the most common cause for apha- with successful recovery compared to those with a less sia was brain infarction, but some more infrequent etiol- favorable outcome (e.g. ). Therefore, we grouped the ogy was also present as for example traumatic brain injury participating patients with regard to aphasia severity. Fur- or subarachnoid hemorrhage. Besides apraxia, neuropsy- thermore, differences in topographic distribution of the chological impairments were mainly from the areas of components identified may give further information attention, memory, executive and visual spatial functions. about functional or dysfunctional changes in brain activa- tion, especially with regard to activation of ipsilesional One-way analysis of variance (ANOVA) revealed signifi- and contralesional processes. cant differences (p < 0.001) between groups for all three clinical aphasia measures. Neither the severe nor the mod- erate aphasia group differed significantly from each other Methods Subjects or the control group with regard to sex, age, years of edu- A total of 20 aphasic subjects were consecutively recruited cation or time post injury (see table 2). from patients admitted to our hospital for rehabilitation. 11 control subjects were recruited from hospital staff and Stimuli non-brain damaged patients of the hospital. All partici- The participants were presented with a syllable detection pants with the exception of two severe and one moderate paradigm using the same natural speech sounds as in our aphasic patient reported to be right-handed. Informed earlier study of automatic syllable discrimination : consent was obtained from all subjects. The study was The frequent standard syllable /ba:/ (p = 0.85) and the approved by the regional research ethics committee of infrequent target syllable /ta:/ (p = 0.15) were presented Eastern Norway. with a stimulus onset asynchrony of 1.5 s in a pseudo ran- domized order with the restriction that two targets could All participants were examined with the auditory compre- not follow each other (see additional file 1, a 30 s sample hension section of the Norwegian Basic Aphasia Assess- of the auditory stimuli). The syllables were digitally ment (NGA; ) and the Token test . These tests recorded from a female, middle-aged native speaker and measure comprehension in relation to both single words cut and re-spliced at zero crossings of the steady-state and short sentences, and with regard to both naturalistic vowel to obtain syllables of same length (/ba:/ = 245.9 objects, body parts, and geometric tokens. In addition, the ms; /ta:/ = 245.2 ms). The recordings of the syllables were patients were investigated with the complete NGA. Fur- low-pass filtered at 8 kHz. The syllables had rise/fall times thermore, all patients were assessed by a neuropsycholo- of 20 ms. A total number of 205 syllables, amongst these gist as part of their routine rehabilitation program. 30 target syllables, were presented binaurally via head- Etiology and lesion location were retrieved from the phones at approximately 80 dB SPL. The participants were patient's medical charts – the latter from descriptions of seated comfortably in a rest chair or their wheel chair and CT or MRI scans. were instructed to press a button with the index finger of their preferred hand as soon as possible when they heard In order to investigate whether different electrophysiolog- the target syllable /ta:/. Since many of the subjects had ical patterns depend on the severity of the auditory com- severe comprehension deficits, the stimuli (up to 15 tar- prehension deficit, the aphasic subjects were distributed gets and 40 standards) were first presented without EEG- into two groups: a group with aphasic subjects with mild recording, and the subject's reaction was observed to or moderate auditory comprehension impairment (mod- assure that the participants had understood the task. Addi- erate aphasia group) and a group of subjects with severe tionally, prior to the recordings for this present study all or very severe auditory comprehension impairment subjects had been presented for the same syllable stimuli (severe aphasia group). The parameter for dichotomiza- in an unattended paradigm  in the same session. tion was a score of 16.5 in the shortened version of the Token test which corresponds to the border between mod- ERP-procedure erate and severe aphasia as described by the authors . EEG was recorded continuously with a sample frequency of 500 Hz and an online band-pass filter with a range Table 1 presents the patients with regard to sex, age, etiol- from 0.05 to 70 Hz at the following electrode sites: Fz, Cz, ogy, lesion site, aphasia type, language functions and neu- Pz, Fp1/2, F3/4, C3/4, P3/4, F7/8, T3/4, T5/6, O1/2, M1, ropsychological impairments. The aphasic subjects and M2. A nose reference electrode was used. The contin- represent a wide range of auditory comprehension uous EEG-data were post-hoc analyzed using band-pass impairment. Global and Wernicke's aphasia dominate the (1 – 15 Hz), zero-phase filtering and ocular artifact reduc- severe aphasia group, while anomia and Broca's aphasia tion using vertical oculograms . Sweeps with ampli- were most common in the moderate aphasia group. In Page 3 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 Table 1: Demographical and clinical data of the aphasic subjects participating in this study. Severe aphasia group a c Sex Years Type of Etiology Site of Months Token NGA NGA Areas of neuropsychological deficits b d e f of age aphasia lesion post injury test comp total F 53 GA BI FT 5,7 1 34 51 apraxia, visual spatial function F 53 GA BI FTP 6,6 2 34 60 memory, visual spatial function F 49 GA SAH FTP 2,5 4 13 35 apraxia, perseveration, problem solving, working memory M 54 WA BI P 4,3 6 46 116 apraxia, executive function, abstract reasoning, visual attention, visual spatial function M 59 GA BI FT 1,7 6.5 57 87 working memory, memory, problem solving M 53 MTA BI P* 3,1 8 55 161 apraxia, memory, problem solving, visual scanning F 48 GA SAH, BI F 4,7 10 54 163 attention, working memory, perseveration M 45 GA MS n.d. 8,9 10.5 48 114 working memory, visual spatial function M 67 WA BI FT* 3,6 11.5 28 107 executive function, problem solving, visual spatial function F 55 WA SAH n.d. 97,7 11.5 51 n.d. attention Moderate aphasia group a c Sex Years Type of Etiology Site of Months Token NGA NGA Areas of neuropsychological deficits b d e f of age aphasia lesion post injury test comp total F 66 TSA BI FT 3,3 19 68 209 memory, visual spatial function M 61 TSA CH FP 2,2 19.5 63 192 attention, executive function, visual discrimination F 63 GA BI FT* 2,7 21 52 165 attention, executive function, memory, abstract reasoning M 61 BA BI FTP 2,1 21.5 65 155 apraxia, attention, problem solving, visual spatial function M 64 TSA CH PO 2,0 22.5 61 191 acalculia, apraxia, working memory, abstract reasoning, visual attention M 41 BA Tumor F 0,8 23 66 185 working memory, visual spatial function resection F 56 AA TBI FP 5,3 28 69 204 apraxia, memory F 65 AA Encephalitis FT** 3,6 30.5 61 202 memory, visual attention F18 AA TBI F, T, P, 3,5 30.5 69 209 attention, executive function, visual scanning O and discrimination M 36 AA BI P 20,6 32 70 n.d. executive function M = male; F = female AA = anomic aphasia; BA = Broca's aphasia; GA = global aphasia; MTA = mixed transcortical aphasia; TSA = transcortical sensory aphasia; WA = Wernicke's aphasia BI = brain infarction; CH = cerebral hemorrhage; MS = Multiple sclerosis; SAH = subarachnoid hemorrhage; TBI = traumatic brain injury F = frontal; T = temporal; P = parietal; O = occipital NGA comp = Norwegian Basic Aphasia Assessment, subsection auditory comprehension NGA total = Norwegian Basic Aphasia Assessment, total score * indicates patients with right hemisphere lesions. ** In addition, this patient had a small lesion in the right temporal lobe. Page 4 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 Table 2: Overview over the three investigated groups. Severe (N = 10) Moderate (N = 10) Control (N = 11) sex (female/male) 5/5 5/5 6/5 age (years) 53.5 (45.1 – 66.9) 53.1 (18.0 – 66.0) 58.2 (33.0 – 74.1) education (years) 12.4 (9 – 15) 14.2 (11 – 20) 13.8 (10 – 18) NGA* aud. comprehension (0 – 71) 42 (13 – 57) 64 (52 – 70) 71 (71) NGA total (0 – 217) 99 (35 – 163) 190 (155 – 209) - Token test (0 – 36) 7.1 (1 – 11.5) 24.8 (19 – 32) 33.6 (31 – 35) time post onset (months) 4.5 (1.7 – 97.7) 3.0 (0.8 – 20.6) - No significant differences in sex distribution, age, years of education or time post onset were found. Mean values are reported, except for time post onset where median is used; minimum and maximum values in parentheses. * = Norwegian Basic Aphasia Assessment tudes exceeding +/- 100 μV in any channel except of the (severe aphasia vs. moderate aphasia vs. control) and the vertical oculogram were excluded from the analysis. within group factors anterior-posterior "line" (frontal vs. central vs. parietal) and "electrode" (5 levels; for example The three left-handed participants had CT-verified right F7, F3, Fz, F4, and F8 for the frontal electrode line). Thus hemisphere lesions and left hemiparesis. For these partic- a significant interaction involving the "electrode" factor ipants, symmetrical and corresponding electrode labels might indicate a hemisphere difference, but would have were swapped between hemispheres. Thus, in this paper to be further analyzed focusing on the relevant electrode odd numbered electrode indices (F3, F7 ...) refer to the contrasts. Greenhouse-Geisser and Bonferroni corrections brain damaged hemisphere (normally the left) and even were applied when appropriate. Latencies were compared numbered electrode indices (F4, F8 ...) refer to the contral- between groups using one-way ANOVAs. esional hemisphere. For the controls – all being right- handed – electrode labels of the left hemisphere are Furthermore, Spearman's rank test was used to analyze referred to as ipsilateral. ERP-amplitudes and latencies for correlations with time after brain-injury, reaction time (RT) and clinical aphasia The standard syllable (/ba:/) waveforms were analyzed for assessment results (NGA auditory comprehension, NGA the N1 component, the responses to the target syllable (/ total, and Token test). Only aphasic subjects were ta:/) for N1 and P3. For each group separately, mean peak included in these analyses, except for the RT-analysis latencies for the components were defined as the mean of where all participants were included. In order to reduce the individual peak latencies located at maxima in the fol- the risk of type I error – on the background of the large lowing time windows: N1 = 60 – 180 ms and P3 = 300 – number of correlation analyses performed – the signifi- 700 ms. Cz electrode was used to define the latencies for cance level for correlations was set to 0.01. standard and target N1, while Pz was used for target P3. For each component respectively, time intervals were cen- Results tered at the relevant group's mean peak latency to calcu- Behavioral results late mean amplitudes. These intervals had a duration of Almost all subjects detected all 30 targets; only three 30 ms for the N1 and 50 ms for the P3 component. Using severe aphasic patients missed one target syllable each. the respective intervals which were derived by the above Many participants had a few false alarms, but none more described procedure, mean amplitudes for the following than four; no significant differences regarding false alarm electrode sites were calculated and further analyzed: Fz, rates were found. These results indicate that the task was a Cz, Pz, F3/4, C3/4, P3/4, F7/8, T3/4, T5/6. A similar anal- rather easy one. ysis was performed separately for the mastoid electrodes (M1/2); these results do not give additional information The target response time was significantly prolonged in and are therefore not reported. the patient groups (p < 0.05): While the mean reaction time was 383 ms in the control group, it was 465 ms in the Furthermore, subtraction waveforms (target - standard) moderate and 586 ms in the severe aphasic group. were analyzed to elucidate the process of discriminating targets from standards. Mean average amplitudes of suc- Standard syllable N1 cessive time windows of 50 ms duration in the range from Grand average waveforms for the three groups respectively 75 ms to 475 ms were calculated and analyzed; this time are presented in figure 1, mean amplitudes and standard span contains the N2 component. deviations for selected electrodes in table 3. Statistical analysis The N1 component was registered as a centrally peaking We analyzed the mean amplitudes using a two-way component with the following mean group latencies and ANOVA model with the between subjects factor "group" amplitudes: control: 115 ms, -7.01 μV; moderate aphasia: Page 5 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 Control -100 0 100 200 300 400 500 600 700 800 ms -2 -4 -6 -8 -10 -1μV 0 Moderate aphasia -100 0 100 200 300 400 500 600 700 800 -2 -4 -6 -8 -10 Severe aphasia -100 0 100 200 300 400 500 600 700 800 -2 -4 -6 Standard Target -8 -10 Difference Gr Figure 1 and average waveforms Grand average waveforms. Vertex grand average waveforms for the standard (green) and the target stimulus (orange) and the difference curve (blue grey) for the three groups respectively. Page 6 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 Table 3: Mean amplitudes electrode group N1 N1 target P3 N2 175–225 ms N2 225–275 ms N2 275–325 ms severe -0,16 (1,02) -1,55 (1,82) 1,43 (4,39) -1,41 (4,26) -1,89 (4,32) -1,98 (3,35) F3 moderate -2,44 (1,43) -1,98 (2,16) 1,67 (2,58) -0,46 (1,96) 0,35 (2,83) 1,61 (3,16) control -3,18 (1,09) -4,04 (1,35) 1,93 (2,99) -3,21 (1,62) -3,57 (3,07) -2,34 (4,77) severe -1,12 (1,26) -1,35 (1,34) 3,11 (4,40) -0,53 (1,94) -0,31 (2,24) -0,11 (3,63) Fz moderate -3,22 (1,44) -2,51 (2,23) 2,80 (3,31) -0,82 (1,99) -0,05 (3,09) 1,70 (3,11) control -4,52 (1,39) -4,92 (1,97) 2,60 (3,87) -3,20 (2,14) -4,84 (3,81) -3,91 (5,13) severe -0,76 (1,12) -1,13 (0,97) 1,98 (3,48) -1,41 (1,64) -1,01 (3,07) 0,17 (3,87) F4 moderate -2,13 (1,72) -2,14 (1,44) 2,36 (3,75) -0,54 (1,45) 0,37 (2,59) 1,78 (3,55) control -3,09 (0,65) -3,54 (1,96) 2,14 (3,66) -1,86 (2,90) -3,26 (3,86) -1,78 (5,46) severe -1,13 (2,16) -2,71 (3,43) 1,82 (3,45) -2,61 (7,36) -1,34 (5,78) -1,68 (4,02) C3 moderate -3,76 (1,38) -3,42 (3,16) 3,52 (3,48) -3,82 (3,51) -0,49 (4,46) 2,80 (3,31) control -5,65 (2,02) -7,05 (2,73) 2,12 (4,23) -7,03 (3,46) -6,87 (4,44) -5,29 (5,96) severe -2,54 (2,12) -2,70 (2,49) 3,03 (4,10) -1,60 (4,35) -0,98 (4,25) -0,94 (4,37) Cz moderate -4,31 (1,30) -2,96 (2,84) 3,94 (3,93) -4,25 (4,64) -1,33 (4,78) 2,51 (3,89) control -7,01 (2,09) -7,20 (3,11) 2,50 (4,20) -5,56 (3,93) -8,87 (6,86) -8,28 (7,36) severe -2,38 (1,96) -3,17 (2,63) 2,89 (3,85) -2,91 (2,83) -2,24 (3,36) -1,11 (4,57) C4 moderate -3,20 (1,74) -3,39 (2,23) 3,63 (3,64) -4,74 (3,62) -2,47 (2,64) 1,40 (3,40) control -5,45 (1,06) -6,02 (2,45) 2,60 (3,94) -5,60 (3,67) -7,68 (5,08) -5,93 (5,61) severe -0,98 (2,20) -2,20 (2,63) 2,06 (3,42) -1,57 (2,79) -0,85 (3,17) -0,73 (3,76) P3 moderate -1,55 (1,10) -1,50 (3,20) 3,47 (3,83) -2,51 (3,26) 0,56 (3,55) 3,67 (4,51) control -3,09 (1,25) -4,02 (2,14) 3,63 (3,61) -6,18 (3,69) -7,25 (4,95) -5,35 (6,38) severe -1,79 (1,81) -3,08 (2,61) 2,60 (4,08) -1,45 (2,83) -1,20 (2,88) -0,71 (4,24) Pz moderate -2,26 (1,18) -2,14 (3,50) 4,58 (3,96) -3,77 (4,10) -0,76 (3,89) 2,90 (5,04) control -4,37 (1,59) -5,22 (2,48) 4,32 (4,25) -6,08 (4,33) -8,54 (6,43) -6,89 (6,94) severe -0,98 (1,59) -2,61 (2,10) 2,83 (3,70) -2,35 (2,42) -2,33 (2,54) -1,25 (4,50) P4 moderate -0,94 (1,00) -1,49 (2,52) 3,38 (3,12) -3,57 (3,59) -1,04 (3,15) 1,65 (4,67) control -2,92 (1,57) -4,29 (2,51) 3,47 (3,81) -6,14 (3,52) -7,77 (4,98) -4,92 (6,03) Mean amplitudes and standard deviations (parentheses) for some selected electrodes for each group respectively. N1 elicited by standard and target syllable and P3 are shown; in addition those intervals from the subtraction wave where significant differences between groups were observed. 115 ms, -4.31 μV; severe aphasia: 110 ms, -2.54 μV (figure zation (~0.4 μV) to the ipsilesional hemisphere and the 2 and 3). The two-way ANOVA revealed a significant severe aphasia group a distinct relative lateralization (~1.2 between groups effect (F [2.28] = 10.67, p < 0.001). Post- μV) to the contralesional hemisphere. This lateralization hoc analysis showed a significant difference between the difference was most prominent in central areas. A ten- control and the severe aphasia group (p < 0.001) and a dency to a significant interaction line * electrode * group marginally significant difference between the control and (F [2, 28] = 2.00, p = 0.076) was observed for an analysis the moderate aphasia group (p = 0.053). of the frontal and central line only. When using a hemi- sphere model with the electrodes F3/4 and C3/4, we A significant line * group interaction was found (F [2, 28] found a significant hemisphere * group interaction = 3.15, p < 0.05). Analysis of each electrode line separately (F [1,28] = 3.38, p < 0.5). indicated that while the group differences were still Target syllable N1 present in all lines, the anterior-posterior N1 distribution varied. The mean N1-amplitudes in the controls were The N1 to the target syllable could be visually distin- evenly balanced frontally and parietally, whereas the guished from the N2 component especially at frontal and moderate aphasia group had larger amplitudes over fron- central sites (figure 5). It peaked about 10 ms later than tal than parietal sites (F [1,9] = 6.40, p < 0.05) and the the N1 elicited by the standard syllable (127 ms, 124 ms, severe aphasia group showed a non-significant tendency and 119 ms for the control, the moderate and the severe for an inverse pattern. Furthermore, the two-way ANOVA aphasia group respectively). The vertex amplitude of the revealed a highly significant electrode * group interaction: target syllable N1 was comparable to that of the standard F [2, 28] = 8.20, p < 0.001, which reflected differences in syllable N1 (see also table 3): -7.20 μV (controls), -2.96 hemisphere distribution of the N1 (figure 4). The controls μV (moderate aphasia), and -2.70 μV (severe aphasia). had an even hemispheric N1 distribution (difference between corresponding electrodes < 0.2 μV) while the Two-way ANOVA showed a significant between group moderate aphasia group showed a minor relative laterali- effect (F [2, 28] = 4.44, p < 0.05) which post-hoc analysis Page 7 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 F7 F3 Fz F4 F8 T3 C3 Cz C4 T4 N1 T5 P3 Pz P4 T6 Control Moderate aphasia -100 100 300 500 700 ms -2 -4 Severe aphasia -6 -8 μ-8 V S Figure 2 tandard syllable waveforms Standard syllable waveforms. Grand average waveforms elicited by the standard syllable /ba:/ for the control (green), the moderate (blue) and the severe aphasia group (red) respectively. revealed to be significant for the control vs. moderate (peak: 419 ms, 4.58 μV). In the severe aphasia group, P3 aphasia comparison (p < 0.05) and marginally significant was somewhat attenuated and peaked over the frontal for the control vs. severe aphasia comparison (p = 0.066). midline (451 ms, 3.11 μV). However, no significant dif- Further analysis of topographic anterior-posterior distri- ferences between groups in P3 mean amplitudes or laten- butions showed the same tendencies as for standard-N1, cies were found. but generally at a non-significant level. Visual inspection indicated a tendency towards the same hemisphere distri- Subtraction curve analysis bution differences as observed for the standard syllable The different time courses and distributions of the sub- elicited N1; a significant electrode * group interaction was traction curves (target - standard waveform) for the three found (F [2, 28] = 4.77, p < 0.001). The severe aphasia groups in successive 50 ms intervals in the time range 75 group showed larger amplitudes over the contralesional to 475 ms are illustrated in figures 6 and 7 (see also table hemisphere especially at central and parietal sites. 3). The negative processing difference of the control group started in the 125 – 175 ms window over left hemisphere P3 temporo-parietal areas and developed into a large, central The P3 component (figure 5, table 3) was observed in the negativity that was registered over the whole scalp and controls as the typical large positivity with a parietal max- lasting until about 325 ms. In the moderate aphasia imum peaking at 436 ms (4.32 μV). A somewhat earlier group, the negative difference started in the same time maximum was observed in the moderate aphasia group window, but had a shorter duration and a more posterior Page 8 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 For the 175 – 225 ms interval, the ANOVA showed a between groups effect (F [2, 28] = 3.67, p < 0.05); post- hoc analysis resulted only in a tendency to significance for the control vs. severe aphasia group comparison (p = 0.062). A significant line * group interaction was found (F [2, 28] = 2.69, p < 0.05). Further analysis of the frontal line resulted in a tendency towards a between group effect (p = 0.089), while we observed a significant difference for the parietal electrodes (p < 0.05). The largest amplitudes -4 at this stage were found parietally in the control group, but centrally in the aphasic groups. For the parietal line, μV we also found an electrode * group interaction (F [2, 28] = 2.48, p < 0.05) with significantly different amplitudes between groups at P3, P4, and Pz electrode site. In this -8 early segment of the processing difference, the control group's negativity was lateralized to the left hemisphere, whereas the moderate aphasia group showed higher amplitudes over the contralesional hemisphere at central -12 and parietal sites. severe moderate healthy aphasia aphasia control The processing difference between target and standard stimulus in the 225 – 275 ms time-window increased – com- Individual N1 mean am Figure 3 plitudes pared to the preceding interval – in the controls, but Individual N1 mean amplitudes. Scatter plot that shows decreased in the aphasic groups. Analysis of variance the individual mean N1 amplitudes in μV (black dots) for showed a between groups effect (F [2, 28] = 10.80, p < each group separately, illustrating between-subject variation. 0.001) which was present between the controls and both Red bars indicate the respective group mean. the moderate (p < 0.01) and the severe aphasia group (p < 0.001). A significant line * group effect was found (F [2, and contralesionally centered maximum. The severe 28] = 4.42, p < 0.01). The processing difference of the aphasia group showed low negative difference amplitudes control group was now centered between Cz and Pz elec- at most electrode sites, but no clear lasting central negativ- trode and centrally localized with regard to hemisphere ity. Analysis of variance revealed significant differences distribution while it still showed larger amplitudes over between groups solely in the three time-windows between the hemisphere contralesional to the brain damage in the 175 and 325 ms which are described in the following. moderate aphasia group. Subject: Neuro scan Subject: Neuro scan Subject: Neuro scan Moderate aphasia Control Severe aphasia EEG file: COpl01.avg SCAN 4.3 EEG file: AFHIpl01.avg SCAN 4.3 EEG file: AFLOPL01.AVG SCAN 4.3 μV Rate - 500 Hz, HPF - 0.05 Hz, LPF - 70 Hz, Notch - 50 Hz Printed : 13:30:32 06-Sep-2006 Rate - 500 Hz, HPF - 0.05 Hz, LPF - 70 Hz, Notch - 50 Hz Printed : 13:30:27 06-Sep-2006 Rate - 500 Hz, HPF - 0.05 Hz, LPF - 70 Hz, Notch - 50 Hz Printed : 13:26:38 06-Sep-2006 + 10.0 + 10.0 + 10.0 +8.8+8.8+8.8 +7.5+7.5+7.5 +6.3+6.3+6.3 +5.0+5.0+5.0 +3.8+3.8+3.8 +2.5+2.5+2.5 +1.3+1.3+1.3 0 0 0 -1 .3 -1 .3 -1 .3 -2 .5 -2 .5 -2 .5 -3 .8 -3 .8 -3 .8 -5 .0 -5 .0 -5 .0 -6 .3 -6 .3 -6 .3 -7 .5 -7 .5 -7 .5 -8 .8 -8 .8 -8 .8 -1 0 .0 -1 0 .0 -1 0 .0 100.00/130.00 ms 100.00/130.00 ms 96.00/126.00 ms μV Topogra Figure 4 phical distribution of the N1 component Topographical distribution of the N1 component. The control (left) and the moderate aphasia group (middle) show an even hemispherical distribution while the N1 of the severe aphasia group (right) is clearly lateralized to the contralesional hem- isphere. Page 9 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 F7 F3 Fz F4 F8 N1 T3 C3 Cz C4 T4 N2 T5 P3 Pz P4 T6 P3 4 Control Moderate aphasia -100 100 300 500 700 ms -2 -4 Severe aphasia -6 -8 -8 μV Target syl Figure 5 lable waveforms Target syllable waveforms. Grand average waveforms elicited by the target syllable /ta:/ for the control (green), the moder- ate (blue) and the severe aphasia group (red) respectively. In the 275 – 325 ms interval, the vertex mean amplitudes of ponents were found for mean amplitudes of the standard the control and the severe aphasia group remained rather stimulus N1 in ipsilesional and midline fronto-central unchanged, while a positive amplitude indicated the start sites and for the mean amplitude of the 325 – 375 ms sub- of a P3 effect in the moderate aphasia group. Also in this traction curve interval in left lateral parieto-temporal sites time-window the processing difference showed a between (table 4). Additionally we found tendencies for correla- group effect (p < 0.01). Post-hoc analysis resulted in a sig- tions (p < 0.05) at other fronto-central sites and also nificant difference between the control and the moderate between the Token test and ipsilesional fronto-central aphasia group (p < 0.01). Line * group (F [2, 28] = 3.37, electrodes. p < 0.05) and electrode * group (F [2, 28] = 3.44, p < 0.05) interactions were significant, and a significant line * For the target stimulus N1, tendencies (p < 0.1) for corre- electrode * group interaction was found (F [2, 28] = 2.24, lations between the Token test and amplitudes at C3 and p < 0.05), but the pattern of electrode differences did not Cz electrode were observed, furthermore between M1 and indicate systematic hemispheric differences. the NGA total score. Correlations ERP-parameters – clinical aphasia measures Correlations with reaction time Correlations between the results from the Norwegian A positive correlation was found between P3 latency and Basic Aphasia Assessment (NGA), i.e. subsection auditory reaction time (r = 0.49, p < 0.01): the later the P3 compo- comprehension and the NGA total score, and ERP-com- nent peaked, the longer was RT. Page 10 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 F7 F3 Fz F4 F8 T3 C3 Cz C4 T4 N2 T5 P3 Pz P4 T6 Control Moderate aphasia -100 100 300 500 700 ms -2 -4 Severe aphasia -6 -8 -10-1 μ0 V Subtraction waveforms Figure 6 Subtraction waveforms. Grand average subtraction waveforms (target /ta:/ - standard /ba:/) for the control (green), the moderate (blue) and the severe aphasia group (red) respectively. Correlations ERP-parameters – time after brain injury the time range from about 100 and up to about 300 mil- Moderate correlations between ERP-amplitudes and the liseconds after stimulus onset indicate differences during time between brain injury and ERP-investigation were on-line stimulus processing or immediately following. found for the N1 component elicited by the standard and These changes were primary stimulus processing reduc- the target syllable (table 4). Mean N1 amplitudes were tion in the form of attenuated N1 amplitude for both smaller, the more time that had passed since brain injury. standard and target stimuli at a latency of about 110 to 120 milliseconds, and a discrimination deficit between targets and standards in the time interval between 175 to Discussion In the present study, we investigated the ability of severe 325 ms post stimulus onset. In this time range a clear N2 and moderate aphasic patients to detect rare target sylla- peak could be identified in the controls, whereas the bles amongst frequent standard syllables and studied the aphasics showed a less distinct negative processing differ- electrophysiological processes involved. The aphasic ence. P3 latency or amplitude did not differentiate groups performed this rather easy task accurately, though between the groups, but was associated with reaction more slowly than the controls. Despite the aphasics' suc- time. N1 amplitude reduction at ipsilesional fronto-cen- cessful task performance, we found several significant dif- tral sites correlated with severity of auditory comprehen- ferences in their electrophysiological processing sion impairment. In addition, N1 amplitude at fronto- indicators. No alterations in ERP latencies were observed, central electrode sites was smaller with increasing time but changes in ERP amplitudes for components found in after injury. Page 11 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 12 12 8 8 0 0 0 μV -4 -4 -8 -8 Control Moderate aphasia -1 -12 2 Severe aphasia -1 -16 6 75 – 12 5 m s 125 – 175 m s 175 – 22 5 m s 22 5 – 2 75 m s 27 5 – 32 5 m s 325 – 37 5 m s 3 75 – 425 m s 4 25 – 475 m s 7 5 – 125 m s 125 – 175 m s 175 – 225 m s 225 – 27 5 m s 2 75 – 325 m s 32 5 – 375 m s 375 – 425 m s 425 – 4 75 m s Subtraction wave, mean Figure 7 amplitudes from time windows Subtraction wave, mean amplitudes from time windows. Mean subtraction amplitudes (target /ta:/ - standard /ba:/) at vertex illustrating the differences between the control (green), the moderate (blue) and the severe aphasia group (red) in time course and size of the N2 component. X-axis: 50 ms time-windows from 75 to 475 ms; y-axis: mean amplitudes in μV. Black bars indicate standard deviation (for graphical reasons only shown in one direction). Significant ANOVA between group effects are indicated: * p < 0.05, ** p < 0.01, *** p < 0.001. Topographic analysis indicated that moderate and severe [29-34,36] and word stimuli [28,42]. A statistical correla- aphasics showed different patterns of brain activation in tion between N1 amplitude and measures for the severity order to solve the discrimination problem. Salient differ- of auditory comprehension measurement in aphasia has ences were that the severe aphasics showed a lateralization not been reported earlier, but in two studies that also of activity focus to the contralesional hemisphere in an dichotomized the aphasic patient groups in relation to early processing window (N1), while showing no evi- auditory comprehension function, a larger N1 reduction dence of discriminatory activation in later time windows. in the severe aphasia groups has been reported [36,43]. The moderate aphasics on the other hand showed a more symmetrical activation in the corresponding early time N1 reduction and its correlations with auditory compre- window with evidence of discriminatory activity in later hension impairment can be interpreted as impaired time windows. The implications will be discussed further sound detection and orienting functions and deficient below. integration of the acoustic properties of speech sounds . Reduced N1 amplitude was found for both the The observed attenuation of the N1 component in the standard and the target syllable which argues for a distur- aphasic groups is consistent with earlier findings for tone bance of primary stimulus processing independent of the Page 12 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 Table 4: Overview of significant correlations N1 Processing difference standard target 175 – 225 225 – 275 325 – 375 NGA auditory F3 (-0.66) comprehension Fz (-0.59) C3 (-0.63) NGA total score F3 (-0.71) T5 (0.63) Fz (-0.63) Time post injury F3 (0.61) M1 (0.69) Cz (0.53) Fz (0.47) F7 (0.64) C4 (0.52) C4 (0.57) Overview of significant correlations between mean amplitudes (N1, processing difference) and auditory comprehension measures or time post injury. Spearman's correlation coefficients for the separate correlations are shown in parentheses. For all correlations: p < 0.01. role of the stimulus in the task. This is supported by the jects, many of whom had sensory-motor deficits involving fact that the discrimination analysis (subtraction wave) the preferred hand. did not reveal differences between groups in the N1 time window, but starting after 175 ms. How can it be explained that the aphasic subjects were able to perform the current task successfully at the same The deviant electrophysiological patterns in the aphasic time as the electrophysiological parameters are signifi- groups between 175 and 325 ms argue for disturbances in cantly attenuated and even correlate with auditory com- the processes of attentional detection of the infrequent prehension measures? A possible suggestion is that syllable /ta:/ and of its classification as the target stimulus. stimulus discrimination in at least some aphasic subjects These differences were found in temporal stages of the N2 was based not on linguistic analysis, but only or mainly waveform which have been identified as being different on purely acoustic features. This strategy is adequate in a between speech sound and purely acoustic processes . task with a very limited set of stimuli and no demands on semantic interpretation, but is not functional in a natural- However, the P3 component was not significantly altered istic comprehension task. Earlier studies have indeed in the aphasic groups indicating no severe impairments of shown that the ability to discriminate phonemes is a nec- target detection and processes of engaging the target reac- essary, but not sufficient condition for the correct identifi- tion; this of course corresponds to the fact that the aphasic cation of these phonemes, and report several aphasic patients were able to detect the target syllables behavio- subjects that could discriminate, but not identify speech rally. The lack of a significant P3 reduction – which con- sounds [5,15]. We would argue that the severe aphasia trasts some results of earlier P3 studies of aphasic patients group, which showed the largest N1 amplitude reduction, – might be due to the large difference between the stimuli has to rely primarily on acoustic analysis. Linguistic and to the relatively low difficulty of the task. In earlier processing – which accounts for parts of the N1 and a studies, the stimuli were rich tones differing in only one more substantial part of the N2 waveform – might thus be parameter: frequency [29,31,36,37] or duration . reduced in these subjects even if these linguistic analyses Actually, the reported P3 attenuation in the aphasic were not necessary to perform the task correctly. In this groups in most of these studies [29,31,36] was not caused perspective, one could furthermore argue that speech by a general processing defect in aphasia, but rather – as sound discrimination based on purely acoustic features the authors noted – by the fact that several subjects were requires more resources and is more exhausting than unable to perform the task; in this present study, even the "normal" speech sound discrimination; this could be sug- very severe aphasic subjects were able to accomplish the gested as one reason why aphasic subjects often report task almost without errors. that listening to language is fatiguing (cf. ). The close relation between the P3 component and the tar- There are some other possible reasons for the observed get response was illustrated by a significant, though weak amplitude reductions. First, compensational pathways correlation between P3 latency and reaction time. might exist in aphasic brains which are not revealed by Although reaction time was significantly prolonged in the ERPs, at least not as recorded in the present study. These aphasic groups, we did not observe P3 latency differences might be processes asynchronous in relation to the stim- between groups. This might be explained by disturbances uli. Alternatively, the N1 and N2 components in healthy in "post-P3" executive motor functions in the aphasic sub- subjects might (partially) be generated by unnecessary, Page 13 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 redundant activity that can be reduced in brain injured guage recovery where the compensational activation of individuals without having impact on brain functions. perilesional areas leads to rather good results, while the Also, one could question the usually proposed sequential contralesional hemisphere can be activated as part of a nature of the processing steps reflected by the N1, N2, and less efficient compensational mechanism. Our results P3 components: Rather, different processes might exist in regarding the N1 component support this hypothesis, and parallel. In injured brains, due to a conflict of resources, we note that the majority of significant correlations early processing steps might then be reduced because task- between auditory comprehension score and single elec- relevant processes are ongoing and prioritized. trode N1 amplitudes are with ipsilesional fronto-central electrodes. However, an important objection to these interpretations of the present results is that the observed electrophysio- The ability to make use of compensational strategies in logical changes might not be due to impaired language speech sound processing probably differs between apha- functions, but rather solely to deficits in purely acoustic sic subjects due to factors as premorbid brain organization processing. On the other hand, one could argue that the and lesion site and size, but also depending on features of amplitude attenuations might be only unspecific effects of the speech sounds that are processed. This variation might brain lesion and lesion size which are not related to apha- be a reason for the complex relation between impaired sia in particular. These problems can be addressed in a speech sound perception and auditory comprehension in study using both a speech sound paradigm and a para- aphasia. digm with purely acoustic stimuli, and furthermore by comparing aphasic patients with brain injured individuals The clinical use of event-related brain potentials in order without aphasia. We are pursuing this approach in an to explore and possibly monitor auditory comprehension ongoing study. in aphasia is under discussion [47-50]. The present study supports the usefulness of event-related potentials in the Some interesting changes in the hemispherical distribu- investigation of processes underlying auditory compre- tion of brain activity were observed: As N1 maximum was hension deficits in aphasia. As this study indicates, ERPs located with an even hemispheric distribution in the con- provide information about central auditory processing trols, the aphasic groups showed two contrasting patterns deficits even in tasks which are successfully accomplished of N1 hemisphere distribution at fronto-central sites: in by the aphasic subjects. Our results regarding the N1 and the moderately impaired aphasic subjects, N1 was evenly N2 waveforms – particularly the significant correlations of distributed or even slightly lateralized to the ipsilesional N1 amplitudes with clinical language comprehension side while it had more relative weight over the non-brain assessment results – suggest that these waveforms deserve damaged hemisphere in patients with severely impaired further attention in the exploration of auditory compre- auditory comprehension. Similar to the results regarding hension impairment in aphasia. the severe group, relatively enlarged N1 amplitudes at contralesional fronto-central sites have been reported Conclusion [30,42]. In a study using monaural stimulation, a similar This study investigated attended speech sound processing pattern was found only for right-ear, but not for left-ear in aphasia recording event-related potentials during a syl- stimulation . lable detection task. The aphasic subjects were able to per- form the task almost without errors, and processes related These findings might be explained by the effect of two dif- to the target identification (P3) were not significantly ferent, but interacting mechanisms: First, a general N1 attenuated. However, electrophysiological components reduction takes place which is directly caused by the brain reflecting primary stimulus analysis (N1) and attended damage and which is larger in those patients with larger stimulus classification and discrimination (N2) indicated brain lesions and more severe impairments, i.e. the severe reduced processing, which constitutes a crucial weakness aphasia group. This attenuation is probably largest over in more complex and naturalistic comprehension tasks. brain damaged areas. Second, different compensational The aphasic subjects might have discriminated the stimuli mechanisms in response to the brain damage might exist: by increased reliance on acoustic differences, and topo- Severely impaired patients activate the contralesional graphic differences between aphasic subgroups and con- hemisphere relatively more than the ipsilesional hemi- trols indicate compensatory changes in activation. The sphere, while patients with lesser impairment show degree to which compensational patterns of speech sound higher activation of the brain damaged than of the cont- processing can be activated probably varies depending on ralesional hemisphere. Thiel et al [38,45,46] have lesion site, time after injury, and language task. reported similar lateralization differences between patients with moderate aphasia and those with more impaired language function and claim a hierarchy of lan- Page 14 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 16. Hickok G, Poeppel D: Dorsal and ventral streams: a framework Competing interests for understanding aspects of the functional anatomy of lan- The author(s) declare that they have no competing inter- guage. Cognition 2004, 92:67-99. ests. 17. Näätänen R, Picton T: The N1 wave of the human electric and magnetic response to sound: a review and an analysis of the component structure. Psychophysiology 1987, 24:375-425. Authors' contributions 18. Näätänen R, Winkler I: The concept of auditory stimulus repre- The study was designed and planned by FB and IR. FB car- sentation in cognitive neuroscience. Psychol Bull 1999, 125:826-859. ried out the data acquisition. Statistical analysis was per- 19. Näätänen R: The perception of speech sounds by the human formed by FB under the supervision of IR. The manuscript brain as reflected by the mismatch negativity (MMN) and its magnetic equivalent (MMNm). Psychophysiology 2001, 38:1-21. was drafted by FB. Both authors read and approved the 20. Roberts TP, Ferrari P, Stufflebeam SM, Poeppel D: Latency of the final manuscript. auditory evoked neuromagnetic field components: stimulus dependence and insights toward perception. J Clin Neurophysiol 2000, 17:114-129. Additional material 21. Pritchard WS, Shappell SA, Brandt ME: Psychophysiology of N200/ N400: a review and classification scheme. Adv Psychophysiol 1991, 4:43-106. Additional file 1 22. Sussman E, Kujala T, Halmetoja J, Lyytinen H, Alku P, Näätänen R: Automatic and controlled processing of acoustic and pho- Speech sound stimuli. A 30 s sample of the task paradigm. netic contrasts. Hear Res 2004, 190:128-140. Click here for file 23. Näätänen R: Attention and Brain Function Hillsdale, New Jersey, Law- [http://www.biomedcentral.com/content/supplementary/1744- rence Erlbaum Associates; 1992. 9081-3-6-S1.mp3] 24. Johnson R Jr.: On the neural generators of the P300 compo- nent of the event-related potential. Psychophysiology 1993, 30:90-97. 25. Linden DE: The P300: where in the brain is it produced and what does it tell us? Neuroscientist 2005, 11:563-576. 26. Picton TW: The P300 wave of the human event-related poten- Acknowledgements tial. J Clin Neurophysiol 1992, 9:456-479. This project has been financed with the aid of EXTRA funds from the Nor- 27. Becker F, Reinvang I: Mismatch negativity elicited by tones and wegian Foundation for Health and Rehabilitation. FB is financed by these speech sounds: Changed topographical distribution in apha- funds, by the University of Oslo and by Sunnaas Rehabilitation Hospital. IR sia. Brain Lang 2007, 100:69-78. 28. Brown CM, Hagoort P, Swaab TY: Neurophysiological Evidence is financed by the University of Oslo. for a Temporal Disorganization in Aphasic Patients with Comprehension Deficits. In Aphasietherapie im Wandel Edited by: References Widdig W, Ohlendorff I and Malin JP. Freiburg, Hochschulverlag; 1. Baker E, Blumstein SE, Goodglass H: Interaction between phono- 1997:89-122. logical and semantic factors in auditory comprehension. 29. Hagoort P, Brown CM, Swaab TY: Lexical-semantic event- Neuropsychologia 1981, 19:1-15. related potential effects in patients with left hemisphere 2. Basso A, Casati G, Vignolo LA: Phonemic identification defect in lesions and aphasia, and patients with right hemisphere aphasia. Cortex 1977, 13:85-95. lesions without aphasia. Brain 1996, 119 (Pt 2):627-649. 3. Baum SR: Consonant and vowel discrimination by brain-dam- 30. Pool KD, Finitzo T, Hong CT, Rogers J, Pickett RB: Infarction of the aged individuals: effects of phonological segmentation. J Neu- superior temporal gyrus: a description of auditory evoked rolinguistics 2002, 15:447-461. potential latency and amplitude topology. Ear Hear 1989, 4. Blumstein SE, Baker E, Goodglass H: Phonological factors in audi- 10:144-152. tory comprehension in aphasia. Neuropsychologia 1977, 31. Swaab TY, Brown C, Hagoort P: Understanding ambiguous 15:19-30. words in sentence contexts: electrophysiological evidence 5. Blumstein SE, Cooper WE, Zurif EB, Caramazza A: The perception for delayed contextual selection in Broca's aphasia. Neuropsy- and production of Voice-Onset Time in aphasia. Neuropsycho- chologia 1998, 36:737-761. logia 1977, 15:371-372. 32. Woods DL, Knight RT, Scabini D: Anatomical substrates of audi- 6. Caplan D, Gow D, Makris N: Analysis of lesions by MRI in stroke tory selective attention: behavioral and electrophysiological patients with acoustic-phonetic processing deficits. Neurology effects of posterior association cortex lesions. Brain Res Cogn 1995, 45:293-298. Brain Res 1993, 1:227-240. 7. Gandour J, Dardarananda R: Voice onset time in aphasia: Thai. 33. Knight RT, Scabini D, Woods DL, Clayworth C: The effects of I. Perception. Brain Lang 1982, 17:24-33. lesions of superior temporal gyrus and inferior parietal lobe 8. Jauhiainen T, Nuutila A: Auditory perception of speech and on temporal and vertex components of the human AEP. speech sounds in recent and recovered cases of aphasia. Brain Electroencephalogr Clin Neurophysiol 1988, 70:499-509. Lang 1977, 4:572-579. 34. Knight RT, Hillyard SA, Woods DL, Neville HJ: The effects of fron- 9. Miceli G, Gainotti G, Caltagirone C, Masullo C: Some aspects of tal and temporal-parietal lesions on the auditory evoked phonological impairment in aphasia. Brain Lang 1980, potential in man. Electroencephalogr Clin Neurophysiol 1980, 11:159-169. 50:112-124. 10. Miceli G, Caltagirone C, Gainotti G, Payer-Rigo P: Discrimination 35. Ilvonen TM, Kujala T, Tervaniemi M, Salonen O, Näätänen R, Pekko- of voice versus place contrasts in aphasia. Brain Lang 1978, nen E: The processing of sound duration after left hemisphere 6:47-51. stroke: Event-related potential and behavioral evidence. Psy- 11. Milberg W, Blumstein S, Dworetzky B: Phonological processing chophysiology 2001, 38:622-628. and lexical access in aphasia. Brain Lang 1988, 34:279-293. 36. Swaab TY, Brown C, Hagoort P: Spoken Sentence Comprehen- 12. Square-Storer P, Darley FL, Sommers RK: Nonspeech and speech sion in Aphasia: Event-related Potential Evidence for a Lexi- processing skills in patients with aphasia and apraxia of cal Integration Deficit. J Cogn Neurosci 1997, 9:39-66. speech. Brain Lang 1988, 33:65-85. 37. Knight RT, Scabini D, Woods DL, Clayworth CC: Contributions of 13. Tallal P, Newcombe F: Impairment of auditory perception and temporal-parietal junction to the human auditory P3. Brain language comprehension in dysphasia. Brain Lang 1978, Res 1989, 502:109-116. 5:13-24. 38. Thiel A, Herholz K, Koyuncu A, Ghaemi M, Kracht LW, Habedank B, 14. Varney NR: Phonemic imperception in aphasia. Brain Lang 1984, Heiss WD: Plasticity of language networks in patients with 21:85-94. brain tumors: a positron emission tomography activation 15. Yeni-Komshian GH, Lafontaine L: Discrimination and identifica- study. Ann Neurol 2001, 50:620-629. tion of voicing and place contrasts in aphasic patients. Can J 39. Reinvang I: Norwegian Basic Aphasia Assessment. In Aphasia Psychol 1983, 37:107-131. and Brain Organization New York, Plenum Press; 1985:181-192. Page 15 of 16 (page number not for citation purposes) Behavioral and Brain Functions 2007, 3:6 http://www.behavioralandbrainfunctions.com/content/3/1/6 40. De Renzi E, Faglioni P: Normative data and screening power of a shortened version of the Token test. Cortex 1978, 14:41-49. 41. Semlitsch HV, Anderer P, Schuster P, Presslich O: A solution for reliable and valid reduction of ocular artifacts, applied to the P300 ERP. Psychophysiology 1986, 23:695-703. 42. Rothenberger A, Szirtes J, Jürgens R: Auditory evoked potentials to verbal stimuli in health, aphasic, and right hemisphere damaged subjects. Pathway effects and parallels to language processing and attention. Arch Psychiatr Nervenkr 1982, 231:155-170. 43. Praamstra P, Stegeman DF, Kooijman S, Moleman J: Evoked poten- tial measures of auditory cortical function and auditory com- prehension in aphasia. J Neurol Sci 1993, 115:32-46. 44. Le Dorze G, Brassard C: A description of the consequences of aphasia on aphasic persons and their relatives and friends, based on the WHO model of chronic disease. Aphasiology 1995, 9:239-255. 45. Heiss WD, Kessler J, Thiel A, Ghaemi M, Karbe H: Differential capacity of left and right hemispheric areas for compensa- tion of poststroke aphasia. Ann Neurol 1999, 45:430-438. 46. Winhuisen L, Thiel A, Schumacher B, Kessler J, Rudolf J, Haupt WF, Heiss WD: Role of the contralateral inferior frontal gyrus in recovery of language function in poststroke aphasia: a com- bined repetitive transcranial magnetic stimulation and posi- tron emission tomography study. Stroke 2005, 36:1759-1763. 47. Csepe V, Molnar M: Towards the possible clinical application of the mismatch negativity component of event-related poten- tials. Audiol Neurootol 1997, 2:354-369. 48. Hyde M: The N1 response and its applications. Audiol Neurootol 1997, 2:281-307. 49. Näätänen R: Mismatch negativity: clinical research and possi- ble applications. Int J Psychophysiol 2003, 48:179-188. 50. Giaquinto S: Evoked potentials in rehabilitation. A review. Funct Neurol 2004, 19:219-225. Publish with Bio Med Central and every scientist can read your work free of charge "BioMed Central will be the most significant development for disseminating the results of biomedical researc h in our lifetime." Sir Paul Nurse, Cancer Research UK Your research papers will be: available free of charge to the entire biomedical community peer reviewed and published immediately upon acceptance cited in PubMed and archived on PubMed Central yours — you keep the copyright BioMedcentral Submit your manuscript here: http://www.biomedcentral.com/info/publishing_adv.asp Page 16 of 16 (page number not for citation purposes)
Behavioral and Brain Functions – Springer Journals
Published: Jan 19, 2007
Access the full text.
Sign up today, get DeepDyve free for 14 days.