J ctt1w8h2wk 17

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Chapter Title: Aphasia as a Temporal Information Processing Disorder

Chapter Author(s): Elzbieta Szelag, Aneta Szymaszek and Anna Oron
Book Title: Time Distortions in Mind

Book Subtitle: Temporal Processing in Clinical Populations
Book Editor(s): A. Vatakis, M.J. Allman
Published by: Brill. (2015)
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chapter 12
Aphasia as a Temporal Information Processing

Disorder
Elzbieta Szelag* ,✝, Aneta Szymaszek* ,✝, and Anna Oron*
1 Introduction
In the Millennium issue of the Brain and Language journal, several articles
emphasised the importance of studying temporal aspects of information pro-
cessing and their close associations with language processing. One article even
stated that “…on space, time and language: for the next century, timing is
(almost) everything” (Osterhout, 2000).
Temporal information processing (TIP) mechanisms have been identified as
the neural basis for many higher cognitive functions, such as language, memory,
new learning, attention, emotional evaluation, motor control, executive system,
planning of activities or decision making. All these functions can be character-
ized by specific temporal dynamics at different ranges of TIP. Such temporal
constraints can be observed both within millisecond and multisecond time
ranges, which create pre-semantically defined (i.e., prior to any semantic evalu-
ation) temporal ‘windows’ for cognitive processing (Pöppel, 1997, 2004, 2009).
Such temporal dynamics appear to be a general property of human cognition. It
provides a structure not only for language, but also for any perceptual or motor
act, as well as any functional state characterized apparently by spatiotemporal
patterns of behaviour, which are evidenced in neuroimaging studies.
Strong experimental evidence supporting this conceptual notion comes from
the language domain in which temporal structure has been well documented by
every day observations of fluent speech, as well as linguistic and psychophysical
data. Using different techniques and populations, experimental studies have
consistently indicated that the left hemispheric superiority for processing verbal
information may reflect more specific control of temporal cues for which human
speech is one example (Szelag et al., 2008, 2011; Wittmann et al., 2004). This evi-
dence can be supported by clinical data, indicating that certain left hemispheric
lesions selectively affect temporal mechanisms (see Table 12.2).
* Laboratory of Neuropsychology, Nencki Institute of Experimental Biology, Warsaw, Poland.

✝ University of Social Sciences and Humanities, Warsaw, Poland.
© Elzbieta Szelag, Aneta Szymaszek, & Anna Oron, 2015 | doi 10.1163/9789004230699_013

This is an open access chapter distributed under the terms of the Creative Commons
Attribution-Noncommercial 3.0 Unported (CC-BY-NC 3.0) License.
Aphasia As A Temporal Information Processing Disorder 329
In the present chapter, we concentrate on language functions, especially on

TIP and acquired language disorders following injuries to the brain, resulting
in aphasia. As many different methodologies have been employed in studies
on TIP, we will also discuss theoretical perspectives in relation to these find-
ings. The purpose of this chapter is to summarize the results of studies
described in the existing literature focusing on TIP in aphasia and to illustrate
these data with the results of our own studies.
2 Language Function
Language is a highly specialized mental function that is a key factor in social

interaction and the evolution of human culture. The broader definition of lan-
guage in Cognitive Neuroscience is “…a symbolic system used to communicate
concrete or abstract meanings, irrespective of the sensory modality employed or
the particular means of expression…” (Purves et al., 2008, p. 511). On the other
hand, human speech can be defined as vocalized concrete acts of language
used in order to communicate (e.g., Price, 2004).
It has been commonly accepted that human language is a complex system,
thus, it is not monolithic. Several language functions or sub-systems are incor-
porated within the framework of network models of language. Accordingly,
language includes spoken (expression) or heard (reception) modalities, com-
munication in writing or reading (visual forms), as well as sign language.
Although verbal output differs significantly among the ca. 6000 languages
existing worldwide, every given natural language contains specific phonology,
vocabulary, grammar, and syntactic rules.
For neurolinguists, the classical dichotomy assumes differentiation between
expression (production) and reception (understanding). Language expression
and our spoken utterances incorporate several processes and sub-functions
involved in the production of the verbal output, such as: conceptual prepara-
tion including planning a sequence of the speech acts, articulation, verbal
fluency, lexicon (lexical encoding), syntax (grammatical encoding), phonology
(phonological encoding), prosody, suprasegmental encoding, pragmatics,
self-monitoring and repair (Blanken et al., 1993). On the other hand, language
reception comprises several processes and mechanisms that allow the listener
to understand the speaker’s communicative intentions, as well as allow the
speaker to understand his or her own speech. The linguistic processing
comprises acoustic-phonetic analysis of the speech signal, phonology (phono-
logical decoding), vocabulary (lexical selection), sentences, syntax (grammati-
cal decoding), and, finally, interpretation of discourse.
330 Szelag et al.
It should be stressed that these processes do not work sequentially one after
another. On the contrary, parallel processing occurs in both speaking and lis-
tening. Direct feedback interactions between particular components of speech
production or speech understanding processes have been heavily debated.
There is only some evidence on the existence of highly limited feedback
from phonological to grammatical encoding in speech production (Blanken
et al., 1993).
Despite diversity of speech sounds, grammar, and syntax among different
mother tongues, some important generalization regarding the neuroanatomi-
cal representation and neural mechanisms underlying language communica-
tion are possible and, thus, reviewed below.
3 Epidemiology, Definitions, and Clinical Syndromes of Aphasia
The term aphasia denotes acquired disturbances of language processing,

resulting from brain damage. Aphasia is a complex language disorder and
refers to deficits apparent in speech, writing or reading, caused by an injury to
brain regions specialized for these functions. This definition contains four cru-
cial aspects, namely: (1) aphasia is acquired; (2) aphasia is a consequence of
brain damage; (3) aphasia affects language processes; (4) other cognitive func-
tions are relatively spared.
Several types of aphasia classification and classes of aphasic syndromes
have been proposed, among other by Luria, Geschwind, Goodglass, Kertesz,
and other researchers. The following are the main aphasic syndromes: global
aphasia, Broca’s aphasia, Wernicke’s aphasia, amnestic aphasia, conduction
aphasia, and transcortical aphasias. The classic location of brain damage in
these aphasia types as well as the main language deficits are summarized in
Table 12.1.
Nowadays, aphasia results predominantly from brain stroke and approxi-
mately 60% of stroke patients suffer from aphasia. The most frequent cause of
aphasia is ischemic infarction in the territory of supply of the left middle cere-
bral artery. Other causes are haemorrhages, tumour, trauma, cerebral infection
or atrophic pathology.
It is estimated that up to 270.000 patients with stroke-related aphasia are
diagnosed worldwide each year (Szaflarski et al., 2011). Only a minority of these
patients recover completely from their language deficits. Examinations of typi-
cal recovery curves reported in the literature have revealed that only 25% of
patients have a chance for full restoration of disturbed language functions.
These data indicate that aphasia still constitutes a major medical and social
Table 12.1 The summary of main language deficits observed in particular aphasic syndromes.
Type of aphasia Classic location of brain damage Particular language functions
spontaneous comprehen- repeti- naming

speech sion tion
Global Extensive damage to the LH, including both anterior and non – fluent impaired impaired impaired
posterior speech areas
Broca’s Inferior part of the premotor cortex (BA 44 and 45) nonfluent preserved impaired impaired
(agrammatism)
Wernicke’s Posterior part of the STG (BA 22) and surrounding cortices fluent impaired impaired impaired
Amnestic Different parts of temporal, parietal lobes, also other areas fluent preserved preserved impaired
of the LH
Conduction Arcuate fasciculus fluent preserved impaired impaired
Transcortical motor Frontal cortex anterior and/ or superior to the Broca’s area, non – fluent preserved preserved impaired
SMA

Transcortical sensory Posterior speech area fluent impaired preserved impaired
Aphasia As A Temporal Information Processing Disorder
Abbreviations: LH: left hemisphere; BA: Brodmann area; SMA: supplementary motor area; STG: superior temporal gyrus.
331
332 Szelag et al.
problem in modern society. This should inspire researchers worldwide to

elaborate new techniques of language rehabilitation.
4 The Neuroanatomical Basis of Language
Current knowledge on understanding cerebral representation of language

comes from 4 main groups of evidence: (1) clinical observations of language
deficits following acquired lesions to the brain; (2) electrophysiological map-
ping of brain areas as an adjunct to various neurosurgical procedures; (3) ‘split-
brain’ studies of patients whose cerebral hemispheres were surgically
disconnected as a treatment of epilepsy; (4) experimental studies employing
many different laboratory techniques (e.g., psychophysical, behavioural,
molecular, biochemical, and neuroimaging).
4.1 Clinical Observations of Language Deficits

An important key generalization is that in the vast majority of individuals the
left brain hemisphere is a primary locus of language communication.
Accumulating evidence has indicated such cerebral representation in 96% of
right-handed and in ca. 70% of left-handed individuals (e.g., Springer and
Deutsch, 1998). Another generalization is that brain areas involved in language
are closely related to the sensory (auditory and visual) and motor regions that
process non-speech signals, as well as generate the non-speech motor acts
(Springer and Deutsch, 1998).
4.2 Electrophysiological Mapping of Brain Areas

Further insight into more detailed mapping of language functions within the
left hemispheric cortical areas comes from electrical stimulation of cerebral
cortex during surgery by Penfield and Roberts (1959). The reason for such sur-
gery is usually brain tumour or searching for epileptic focus before removing
diseased brain tissue. Such stimulations were performed in awake and con-
scious patients and allowed the surgeon to localize cortical areas that interfere
with speech during stimulation. These observations allowed exact location of
language and indicated that several left hemispheric regions control different
language functions. These large regions are usually outside the ‘classic’ lan-
guage area described by Paul Broca and Carl Wernicke in the late 1800s (Blanken
et al., 1993). Despite individual differences in the borders of the region support-
ing language, it comprises usually parts of the left hemispheric frontal, tempo-
ral, and parietal lobes, specifically, large regions of perisylvian cortices for both
language production and comprehension.
4.3 ‘Split-brain’ Studies

Commissurotomy refers to complete surgical sections of the corpus callosum,
anterior commissure, dorsal, and ventral hippocampal commissures and, in
some cases, the massa intermedia. It resulted in total isolation of cortical areas of
two hemispheres. Following complete cerebral commissurotomy, the clear hemi-
spheric specialization was observed as the ‘split-brain’ phenomenon p rovided
clear evidence on independent contribution of each hemisphere to language
processing as well as special behaviour and capacity of isolated hemispheres.
In summary, the left hemisphere represented language competence
observed in speaking, hearing, reading or writing, but some limited right hemi-
spheric capacities in language comprehension and production were also evi-
denced (Zaidel, 2001; Zaidel et al., 2003).
4.4 Experimental Studies

The results of detailed mapping of language functions derived from brain
stimulation during surgery were further supported by non-invasive brain
imaging techniques, using electrophysiological methods, positron emission
tomography (pet), functional magnetic resonance imaging (fMRI), magneto-
encephalography (meg) or suppression of language functions during transcra-
nial magnetic stimulation (tms). All these modern techniques showed activity
of various areas in different language tasks, indicating a broader picture of the
way language is processed.
4.5 Summary of Cortical Regions Supporting Language

A detailed characteristic of cerebral representation of language is beyond the
scope of the present chapter but has been described for example by Scott
(2012) and Turken and Donkers (2011). We summarized briefly the main role of
cortical regions supporting language communication, focussing only on
clinical-pathological data of patients with lesions of the specific brain areas.
Next, we referred these clinical data to the neural basis for language produc-
tion and comprehension. It is evident that the clinical data were further con-
firmed by results of modern neuroimaging studies. Such approach is justified
by the topic of the present chapter in which we concentrate on the dissocia-
tion between different ranges of TIP or ‘temporal windows’ (i.e., processing of
information within millisecond vs. multisecond time domains) in case of
expressive and receptive deficits observed in particular aphasia types. In this
approach, therefore, we concentrate on the left frontal lobe where the motor
functions are carried out controlling language expression, as well as on
the left posterior regions of the temporal lobe in which the auditory func-
tions are represented, controlling language reception. Moreover, in language
334 Szelag et al.
communication subcortical structures are involved, e.g., basal ganglia, insula,

cingulate gyrus or cerebellum, as well as other structures supporting writing,
reading, verbal memory, word finding, repetition, verbal fluency, programming
of longer verbal utterances, affective control, and articulation. The right hemi-
spheric contribution seems also important.
The neural basis for producing language comprises Broca’s area, i.e., inferior
part of the premotor cortex (inferior frontal gyrus) of the left frontal lobe. This
region includes Brodmann areas 44 and 45. Initial evidence on the involvement of
this region in producing language was provided by the French anatomist and neu-
rologist – Paul Broca in 1861. He described a patient who suffered from acquired
brain damage to this region, resulting in disability to produce fluent speech. The
lesion’s location was confirmed by Broca in post-mortem brain examination.
The importance of this region is vividly evidenced in patients suffering from
motor aphasia (other names: efferent motor aphasia, Broca’s aphasia, produc-
tion aphasia, or nonfluent aphasia), a common neurologic disorder, resulting
in inability to organize and control the linguistic content of the utterance with
relatively preserved auditory comprehension. The typical patient suffering
from a lesion in the Broca’s area cannot express thoughts appropriately,
because of the loss of the meaningful fluent verbal output, reduced phrase
length (so called ‘telegraphic style’ of the verbal output) and agrammatism, i.e.,
disrupted rules of grammar and syntax, even though the verbal apparatus and
articulatory movements remained intact.
The core symptom in Broca’s aphasia is a disruption of brain mechanisms
responsible for producing phonemes, as well as combining phonemes into
morphemes and words into sentences. Thus, in Broca’s aphasia the efferent
pathway from the Broca’s area to the peripheral articulatory apparatus is dis-
rupted. Generally, such patients produce structurally incorrect utterances, non-
sense syllables, transpose words with some sensible meaning. Thus, a listener
may have an impression that the patients knew what they intended to say.
Broca’s aphasia encompasses interactions of several impairments, including
defects in linguistic formulation, motor programming, initiation and mainte-
nance of verbal output, and affective control. Thus, selective damage to the
posterior inferior frontal cortex does not produce the full motor syndrome, but
rather Broca’s aphasia is caused by extensive damage to several neighbouring
frontal regions.
On the other hand, an important contribution indicating the neuroana-
tomical basis of language comprehension was made first by the German psy-
chiatrist – Carl Wernicke in 1874. He described for the first time a patient who
produced fluent utterances with appropriate grammar and syntax, but could
not understand heard (or written) communications addressed to him by other
speakers. These deficits were caused by damage to the left hemispheric tempo-
ral lobe, more specifically, to the posterior part of the superior temporal gyrus,
which is referred to, in honour of its discoverer, as Wernicke’s area. According
to the Brodmann map it comprises area 22, but often also surrounding tempo-
ral and parietal cortices. The lesions in this part of the brain caused Wernicke’s
aphasia (other names: receptive aphasia, sensory aphasia or fluent aphasia).
In contrast to Broca’s aphasia, patients suffering from lesions affecting
Wernicke’s area cannot understand the speech of other people, as well as their
own speech. As a consequence, utterances generated by such patients have little
(or even not at all) sense because phonemes, syllables, and words are not cor-
rectly linked. In more severe forms of this disorder, the verbal output is named
‘jargon aphasia’, as the listener cannot understand it at all. Wernicke’s aphasia
can be characterized by fluent speech, adequate syntax and grammar, but inap-
propriate choice of words (paraphasia) and little spontaneous repetitions. A
core symptom of Wernicke’s aphasia is disruption of phonemic hearing, i.e., the
ability of analysis and synthesis of speech sounds (phonological decoding). For
example, a patient with such disruption cannot properly decode phonemes
(consonants and vowels) and, as a consequence, is not able to properly decode
words and sentences. The impaired phonological hearing results, therefore, in
disordered comprehension. The schematic description of classic aphasic syn-
dromes is given in Figure 12.1 (compare also Table 12.2 and Section 7, below).
Figure 12.1 The differential diagnosis of main aphasic syndromes.
Table 12.2 Summary of results reported in the existing literature regarding deficient temporal processing in aphasic patients.
336
No Author Subjects Method Results Conclusions
Evidence from milliseconds timing

1 Efron, 1963. n = 16: Stimuli: 100 % correctness was achieved in
6 motor AP; visual: paired 5ms pulses of either red or nc for isi s from 62 to 162ms and in
4 receptive AP; green light presented in rapid succession; ap for ISI from 162 to 600ms.
1 unclassified AP; auditory: paired 10ms tones (250Hz and Worsened performance in motor
5 nc. 2500Hz) presented with 13 different ISIs AP on the auditory task, in receptive
varied from 0 to 600ms; ap on the visual task.
Task:
to report which stimulus in the pair was
the first one.
2 Swisher & n = 30: Stimuli: nc: Affected timing,
Hirsh, 1972. 10 ap with lh visual: paired diodes presented in rapid tot = 20ms for stimuli presented at depending on
damage; succession at the same or different places different places; the subject

5 non ap with rh (yellow- blue; yellow- yellow); tot = 30 – 40ms for stimuli group.
damage; auditory: paired clicks presented presented at the same place;
15 nc . monaurally, tones (300 Hz, 3000 Hz) fluent ap : required the longest gap
presented binaurally. The stimuli were to order stimuli, especially the
presented with soas varied from: 20 to auditory ones;
640ms; non ap : no deficits on the visual
Task: tasks, but required longer intervals
Szelag et al.
to report which stimulus in the pair was to order tonal stimuli.

the first one.
3 Tallal & n = 26: Stimuli: isi of 428ms: no group differences;
Newcombe, 10 AP with lh paired 75-ms complex tones composed isis from 8 to 305ms: poorer
1978. damage; of frequencies within the speech range performance in AP than in other
10 non AP with rh and presented in rapid succession with groups.
damage; different isis;
6 nc. Task:
to report the order of stimuli presented
in a pair.
4 v. n = 65: Stimuli: Fluent AP: increased tot in Affected timing,
Steinbüchel 7 non – fluent AP paired 1-ms clicks presented monaurally; comparison to all other groups. depending on
et al., 1999a. with lh damage; Task: the subject
16 fluent AP with lh to report the order of stimuli presented group.
damage; in a pair.
9 non AP with lh
damage;
8 non AP with rh
pre – central damage;

8 non AP with rh
post – central
damage;
17 nc.
5 v. n = 62: Stimuli: Fluent AP: increased tot in
Steinbüchel 7 non – fluent AP paired 1-ms clicks presented comparison to all other groups.
337
et al., 1999b. with lh damage; monaurally;

Table 12.2 Summary of results reported in the existing literature regarding deficient temporal processing in aphasic patients (cont.)
338
14 fluent AP with lh Task:

damage; to report the order of stimuli
9 non AP with lh presented in a pair.
damage;
9 non AP with rh pre
– central damage;
6 non AP with rh
post – central
damage;
17 nc.
6 Wittmann n = 30: Stimuli: Fluent AP: increased tot in
et al., 2004. 6 non – fluent AP paired 1-ms clicks presented comparison to all other groups.
with lh damage; monaurally;

12 fluent AP with lh Task:
damage; to report the order of stimuli
6 non AP with rh pre presented in a pair.
– central damage;
6 non AP with rh
post – central
damage.
Szelag et al.
7 Fink et al., n = 38: Stimuli: AP: increased tot in both tasks. Affected timing,
2006. 8 anomic AP; Exp. 1 – paired 1-ms clicks presented depending on
2 Wernicke’s AP; monaurally; the subject
4 Broca’s AP; Exp. 2 – paired tones of 800Hz and group.
5 non- classified AP; 1200Hz presented binaurally;
19 nc. Task:
Exp. 1, 2 – to report the order of
presented stimuli.
8 Stefanatos n = 13: Stimuli: AP: impaired gap detection task. Affected timing
et al., 2007. 5 Broca’s AP; noise segments modelled after formant in in all groups of
7 anomic AP; speech of different length, separated by a AP.
1 Wernicke's AP. silent gap of 10, 20, 40, or 80ms duration;
Task:
to detect the gap between stimuli and
ascertain if two stimuli were the same or
different.
9 Sidiropoulos n = 6: Stimuli: AP: Affected or

et al., 2010. 1 conduction AP with Exp. 1 Exp. 1 – intact temporal resolution preserved
both lh paired two noise segments of identical in ‘intra- channel condition’; timing in AP,
ischemic infarction spectral energy distribution (‘intra- Exp. 2 – reduced performance in depending on
and an older, channel condition’); ‘inter- channel condition’. the experiment.
contralateral parieto – Exp. 2
occipital cerebrovas- pairs of different noise segments:
339
cular lesion; broadband and filtered noise of different

5 nc. length (‘inter- channel condition’);
340
Task:
Exp. 1 – to detect the gap
between two identical noise segments;
Exp. 2 – to detect the gap
between pairs of different noise
segments.
Evidence from multiseconds timing
10 Szeląg et al., n = 56: Stimuli: Broca’s AP: disrupted temporal Affected timing
1997. 6 Broca’s AP with LH metronome beats presented at 9 integration evidenced by a different only in Broca’s
pre – central damage; different frequencies; strategy in mental accentuation AP.
14 Wernicke's or Task: based on counting;
amnestic AP with lh to accentuate mentally every 2nd, 3rd or Other groups: a combination of
post- central damage; other beat to create subjective rhythmic mental counting and constant time

9 non AP with lh patterns. strategies.
damage;
6 non AP with rh pre
– central damage;
6 non AP with rh
post – central
damage;
Szelag et al.
15 nc.
11 v. n = 65: Stimuli: Exp. 1: longer duration of spontane- Affected timing
Steinbüchel 7 non – fluent APExp. 1 ous reversal rate in patients than in in AP in both
et al., 1999a. with LH damage; visual: ambiguous figures: Necker Cube nc; hundreds of
or Rubin Vase;
16 fluent AP with lh Exp. 2: AP apply integration by milliseconds
damage; auditory: tones of different frequencies, counting differently than all other and a few
9 non AP with lh reversible syllables; groups; seconds time
damage; Exp. 2 Exp. 3: impaired self- paced tapping domains.
8 non AP with rh metronome beats presented at 9 tempo in AP;
different frequencies;
pre – central damage; Exp. 4: no differences between
8 non AP with rh Task: patients and nc in a maximum
post – central Exp. 1 – to press a button at each tapping tempo.
damage; perspective switching for a presented
17 nc. ambiguous figure;
Exp. 2 – to accentuate mentally every
2nd, 3rd or other beat to create a
subjective rhythmic pattern;
Exp. 3 – to tap in a self- paced tempo;

Exp. 4 – to tap in a maximum tempo.
12 Wittmann et n = 61: Task: Exp. 1: impaired in AP; Affected timing
al., 2001. 22 AP with lh damage; Exp. 1 – to tap in a self- paced tempo; Exp. 2: no differences between in AP in
14 non AP with rh Exp. 2 – to tap in a maximum tempo. patients and nc. hundreds of
damage; milliseconds
9 non AP with lh time range.
341
subcortical damage;
16 nc.
342
13 Kagerer et al., n = 43: Stimuli: No differences between patients and Affected timing
2002. 5 Broca’s AP; visual: nc in reproduction of short intervals in non AP with
10 Wernicke’s, 1.green oblong of 80 x 50 cm2, with equal (1000 – 2500ms); rh damage in a
amnestic AP; luminance Impaired reproduction of long few seconds
9 non AP with lh 2.19th century painting depicting a intervals (3000 – 5500ms) in non AP time range.
damage; pastoral scene with rh damage both pre- – and post
5 non AP with rh auditory: – central, in comparison to other
pre- central damage; 1. 500 Hz tone groups.
5 non AP with rh 2. noise of running water
post – central Stimuli presented in blocks with different
damage; standard intervals varied from 1000ms to
9 nc. 5500ms.
Task:

to reproduce standard interval.
Abbreviations: LH – left hemisphere, rh – right hemisphere, ap -aphasic patients, non ap – non aphasic patients, nc – normal controls, tot – temporal –
order – threshold, isi – inter – stimulus – interval, soa – stimulus – onset – asynchrony
Szelag et al.
Despite the general features of neuroanatomical basis of language described

above, a vast number of subsequent studies using various methods have con-
firmed the contribution of many additional areas of both hemispheres, as well
as subcortical structures to verbal communication.
Taking into account the other language-sensitive regions, the traditional
model of language representation assuming two well-defined parts supporting
expression and reception needs to be modified. Although it seems very useful
in the clinical practice and there is a number of evidence supporting such dis-
sociation of language function, the current thinking on the traditional model
of language is undergoing some fine-tuning, considering three groups of evi-
dence: (1) neuroimaging data indicating the involvement of many other brain
regions, beside the Broca’s and Wernicke’s areas, in language communication;
(2) individual differences in representation of language production and recep-
tion far beyond the Broca’s and Wernicke’s area; (3) neuroanatomical represen-
tation of various language functions (see above) and phenomena, like
bilingualism or sign language.
For instance, using neuroimaging it is possible to define the exact areas
damaged by stroke or trauma and to relate these structural lesions to deficient
language functions, which often do not cover the deficits expected by the tra-
ditional model. Moreover, data from individual patients indicated that lesions
to the Broca’s area not always led to Broca’s aphasia. The deficits characteristic
for this syndrome were also observed in case of brain damage to many other
brain regions far beyond the region traditionally associated with the produc-
tion of speech. Similar observations concern Wernicke’s aphasia and disrupted
auditory comprehension. It is interesting to note that brain imaging techniques
(mri, fMRI or pet) have revealed that anatomical damage does not necessarily
cover the functional damage, which usually extends beyond the border of
structural damage. At this point it should be mentioned that these neuroimag-
ing techniques can map brain activity, but not necessarily linguistic function
directly.
In summary, many brain regions control language communication. It would
be a question for further studies what is their contribution to particular lan-
guage functions for verbal communication, moreover, to what extent these
areas are specific to language. To answer these questions, many psycholinguists
seem to concentrate not only on the structures (localization) of particular lan-
guage functions, but also on the neural mechanisms underlying language pro-
cessing in real time, thus, on the temporal structure of linguistic processing.
Focusing on temporal mechanisms underlying different language functions
would allow us to understand temporal coordination, segmentation and inte-
gration involved in expression and comprehension. In this approach, studies
344 Szelag et al.
on TIP in different time domains can indicate the activity of the dynamic net-
work in which human language is rooted in norm and pathology. If the activity
of the timing mechanisms operating at different ranges differs reliably in
patients and controls, it may interfere with the associated mental activity.
5 Temporal Constraints of Speech
Both everyday observations and experimental data indicate temporal con-

straints of human speech. Its temporal organization is multileveled. There is
strong evidence supporting the thesis that our language communication is
rooted in TIP, i.e., in temporal ‘integration’ and temporal ‘chunking’ or ‘seg-
mentation’ on several time scales. One can distinguish the milliseconds
(shorter time scale) and multiseconds (longer time scale) temporal constraints,
which are controlled by a high- or low-frequency processing system, respec-
tively (Pöppel, 2004; Szelag et al., 2004; Szelag, 2011). The former system con-
cerns predominantly phonological encoding/decoding and syllabification,
whereas the latter one concerns rather lexical selection and sentence produc-
tion/reception.
It is important to note that language is not an isolated system, therefore,
similar time scales can be distinguished in several key aspects of our behav-
iour, e.g., in motor control, as well as in many other mental functions which are
strongly related to speech expression and/or reception (Pöppel 1997; Szelag et
al., 2009). Therefore, we are of the opinion that timing is a critical factor for our
verbal communication and provides an important insight into how the brain
parses language in norm and pathology.
It is commonly known that normal production and understanding of lan-
guage involves highly skilled coordination of several processes. Similar tempo-
ral levels or ‘processing platforms’ are incorporated in both speech expression
(encoding) and reception (decoding). In phonological encoding, for instance,
we produce the phonological forms, in particular, their segmental structure.
Thus, central to phonological encoding are phonemes or syllables as the basic
units for articulation produced by the speaker successively. On the other hand,
in phonological decoding these phonological forms have to be perceived by the
listener. Thus, these strings of successive phonemes and syllables perceived by
the listener are also central to phonological decoding and speech reception.
The processing of temporal information in the speech signal has been inves-
tigated explicitly over the last few decades. The high-frequency processing sys-
tem, i.e., a time domain of some tens of milliseconds, seems to be relevant to
phonemic awareness (labelled also as phonemic hearing). It is defined as a
unique human ability to analyse and synthesise speech sounds. These pro-
cesses are fundamental with respect to auditory comprehension. In the time
platform of about 20–40ms, information about the place of articulation in stop-
consonants (p, b, t, d etc.) is contained. Formant transitions, characterized as
short sound waveforms that change frequency across a time interval of ca. 40ms
vary, according to the place of articulation. Spectrographic analyses of our ver-
bal utterances clearly indicated that rapid formant transitions in stop-
consonants (p, b, t, d etc.) are limited in time up to 40ms. Because of the specific
structure of our articulators these stop-consonants cannot be prolonged in the
fluent speech because a forthcoming vowel sounds immediately.
On the other hand, fricatives (w, f, s, z etc.) or vowels (a, o, u etc.) are charac-
terized by a structure less limited in time and can sound in the fluent speech
much longer, even up to 200ms. Despite important individual differences in
the speech expression rate, particular speech sounds come on average as fast
as 10 to 15 phonemes per second. The temporal structure of the verbal output
is usually automatic (controlled by procedural memory) and often happens
without any attentional or motor control of ‘how’ we say things. In contrast,
‘what’ we say is fully consciously controlled.
Another example of temporal constraints with respect to phonemic aware-
ness on the millisecond time scale comes from the Voice-Onset-Time (vot)
paradigm. In the perception of voicing contrasts of stop-consonants in sylla-
bles like DO vs. TO, a difference in duration of about 40ms between the burst
of the air and the onset of laryngeal pulsing in articulation of the initial conso-
nant, is defined as the vot. It distinguishes voiced (/b/, /d/, /g/ etc.) from voice-
less stop-consonants (e.g., /p/, /t/, /k/ etc.).
Such evidence supports the thesis that the high-frequency processing sys-
tem is related to phoneme processing and phonemic hearing, thus, the crucial
processes with respect to auditory comprehension.
Furthermore, there exists the low-frequency processing system, corresponding
to the time range of a few seconds, which is related to the duration of sentences
in fluent speech. For example, our average syllabic rate is ca. 3–4 per seconds,
whereas words are usually articulated at a speed of approx. 2 per second. At this
rate we are able to retrieve lexical items from a mental lexicon that on average
contains probably tens of thousands items. Although there are some so-called
‘fast speakers’ who are able to produce even up to 7 words per second, it is usually
difficult to follow such fast speech tempo, which does not fit the typical tempo.
Another source of evidence comes from analysis of the temporal structure
of fluent speech in many languages, like Polish, Russian, German, English or
Chinese (Pöppel, 1997). Several data have indicated that in many languages
the duration of phrases in fluent speech is limited in time up to a few seconds.
346 Szelag et al.
Thus, spontaneous flow of speech is temporally segmented or ‘chunked’ in a

few seconds time domain. This phenomenon is called ‘semantic parsing’.
Usually, particular phrases are followed by hesitation pauses that are necessary
both for the listener to process the information provided by the speaker, as well
as for the speaker to prepare the next phrase.
At this point it seems interesting to note that similar temporal segmenta-
tion as observed in oral language has been confirmed in sign language. In such
way of communication, consecutive signs (i.e., motor acts) are grouped within
segments of a few seconds duration, followed by pauses when signs are not
provided. The duration of particular signed segments corresponds to those
observed in oral language, described above, with a little shorter durations of
ca. 2s in sign language. The similar temporal chunking of speech expression,
independently of the kind of articulation (using either the oral output or hand
movements) suggests the existence of a common neural mechanism control-
ling human language communication, independently of the output from the
system.
To summarize, both the millisecond and multisecond time ranges are cru-
cial for our language communication. Hence, authors are of the opinion that
the left hemispheric specialization for language derives from specialization for
timing. Furthermore, language deficits of various etiologies in children and
adults have been associated with timing disorders on both mentioned time
scales. Language processing depends, thus, on temporal constraints of the
brain on several levels, which may be affected after the brain injury.
In the traditional view different language disorders (e.g., aphasia, specific lan-
guage impairment) or reading and writing disorders (dyslexia) have been
viewed as distinct clinical syndromes. Recently, this viewpoint has been refor-
mulated because of a close link between these syndromes. Neuropsychological
profiles taking into account the coexistence of specific temporal processing
disorders and phonological impairments show some similarities between par-
ticular syndromes. In general, they are characterized by deficient TIP in both,
the millisecond and multisecond ranges. Because of the central relevance of TIP
to our understanding of the neural basis of cognitive systems, one may define a
typical TIP and abnormalities in such processing in human populations suffer-
ing from impaired cognitive function (Szelag and Skolimowska, 2012).
6 Deficits in Processing Temporal Information in Aphasic Patients
Studies of patients suffering from aphasia following left hemispheric brain

damage provide an important contribution to our understanding of TIP.
The first evidence of this type was provided by Efron (1963) and later by Swisher
and Hirsh (1972). They observed that aphasic patients displayed parallel defi-
cits in both speech comprehension and rapidly changing temporal
information.
These observations were confirmed in several further reports, including our
own studies. Table 12.2 summarized the results of studies conducted using dif-
ferent patient populations and experimental techniques. Looking at Table 12.2,
we may conclude that TIP within both the millisecond (points 1–9) and multi-
second (points 10–13) time ranges is usually disturbed in patients with aphasia
following left hemispheric brain damage.
There exist also some experimental evidence on the high frequency pro-
cessing system in normal healthy volunteers. These studies are often focussed
on temporal order of incoming events and measurement of temporal-order
threshold. It reflects an ability to perceive the relation before-after for stimuli
presented in rapid succession in order to be brought into a sequence by
approximately the same value of some tens of milliseconds for visual, auditory,
and tactile modality (Hirsh and Sherrick 1961; Kanabus et al., 2002; Zampini et
al., 2003, 2005). The correspondence of this value across different senses sug-
gests a common central mechanism for vision, hearing or touch and it may be
concluded that the neural process underlying sequential ability is activated to
identify primordial events, independently of the sensory modality (Pöppel,
2009). Such ability allows us to reduce complexity of incoming events, which
stimulate incessantly our senses, and to create our conscious percepts.
Strong experimental evidence provided in Table 12.2 (points 1–9) may sug-
gest a disruption of this high-frequency process following left hemispheric
brain damage, resulting in disordered language communication, as a conse-
quence of primordial event disruption. Moreover, the data on temporal con-
straints of human speech on the milliseconds level discussed in the previous
section have indicated the importance of this time platform with respect to
speech reception. Hence, disordered processing of information on this level
following brain injury may underlie language problems, especially, problems
in phonemic hearing and auditory comprehension. These problems often con-
stitute a core symptom after posterior lesions to the left hemisphere, resulting
in receptive aphasia (see above for aphasia classification).
On the other hand, Table 12.2 presents also data indicating deficient timing
on low frequency processing, i.e., in the domain of hundreds of milliseconds or
a few seconds (points 9–13). Considering temporal constraints of speech (see
Section 5), the former time window is related to the level of syllables, whereas,
the latter one may be important with respect to the fluent verbal output and
expression of phrases and sentences. It requires the ordering of successive
348 Szelag et al.
syllables and words into logic strings, which build fluent utterances and pro-
vide a structure for language communication.
According to the hierarchical model of time perception proposed by Ernst
Pöppel (1997, 2004; Szelag et al., 2004), the existence of temporal integration on
a few seconds scale creates a high-frequency level of complexity reduction. In
fact, in fluent verbal communication we usually do not concentrate so much
on particular phonemes, syllables or words, but on logic utterances of what we
say or what we hear. Thus, the primordial events identified on a level of higher
temporal resolution (some tens of milliseconds) are next sequentially linked
together into a perceptual ‘gestalt’, representing an operating range of a few
seconds. This process is also labelled in the literature as ‘temporal binding’ or
‘temporal integration’ and it is expected to be important for our conscious
experience, of which verbal communication may be one example.
Although reports on TIP on the supra-second level are fewer, Table 12.2
shows that using different experimental paradigms, like subjective accentua-
tion of metronome beats (points 10–11), spontaneous reversal rate of ambigu-
ous figures (point 11), finger tapping in a self-pace and maximum tempi (point
12) or reproduction of temporal intervals (point 13), a disruption of temporal
binding can be observed, which has been also evidenced following injury to
the brain, predominantly to the anterior parts of left hemisphere, resulting in
motor aphasia. The patients suffering from this syndrome had deficient bind-
ing operations that probably underlie problems with the fluent verbal output
(i.e., effortful, nonfluent speech, compare above), but also some comprehen-
sion deficits, especially for longer utterances, which need to integrate and hold
the incoming information for a few seconds.
To sum up, acquired language disorders following brain damage are strongly
related to deficient timing on several levels, which create a neural timeframe
for verbal communication. Thus, the superiority of the left hemisphere for the
processing of verbal information may reflect more primary specialization for TIP.
7 Relationships between Disrupted Timing and Specific Aphasia

Syndromes
It seems also interesting to note, that in our studies on disrupted timing in

aphasia, an important dissociation between specific language deficits (in pho-
nemic hearing vs. effortful nonfluent verbal output) and temporal deficits
(at the sub- or supra-second level) were observed (v. Steinbüchel et al., 1999b;
Szelag et al., 1997; Wittmann et al., 2001). Specific left hemispheric lesions
selectively damaged temporal mechanisms operating either within the milli-
second or multi-second time scales (Table 12.2, points 4–6, 10–12). The former
range was assessed with auditory temporal-order-threshold (Figure 12.2

whereas, the latter one with subjective accentuation paradigm, which corre-
sponded to the upper limit of the temporal integration mechanism, operating
in a time window of a few seconds (Figure 12.3). In patients with left hemi-
spheric post-central lesions, suffering from Wernicke’s aphasia (characterized
by deficits in phonemic hearing and poor comprehension), deficient tempo-
ral-order-thresholds were reported (Figure 12.2). Those patients needed a sig-
nificantly longer gap between successive events to correctly report their
before-after relation. These timing deficits corresponded to their language
Figure 12.2 Auditory order thresholds (mean and standard deviations) for the five patient
groups with focal brain injuries and for an orthopaedic control group are
shown: lh. pre-anterior left hemisphere (pre-central) with non-fluent aphasia;
lh. post-posterior left hemisphere (post-central) with fluent aphasia (*p<1%
for group differences as compared with controls and L. noAph; statistical
calculation with Scheffe post-hoc test); L. noAph-left-sided subcortical
lesions without aphasia; rh. pre-anterior right hemisphere (pre-central); rh.
post-posterior right hemisphere (post-central). Reprinted from Neuroscience
Letters, 264, v. Steinbüchel N., Wittmann M., Strasburger H., Szelag E. “Auditory
temporal-order judgment is impaired in patients with posterior regions of the left
hemisphere” 168–71.
Copyright (1999) with permission from Elsevier
350 Szelag et al.
Figure 12.3 The measured integration interval length (miil) plotted against the metronome
frequency using three different strategies in Broca’s aphasia and other patients.
Integration (A) by time; (B) by number; (C) in Broca’s aphasic patients; (D) in all
the remaining patients. Standard deviation values (in ms) for the consecutive
frequencies in the Broca’s aphasic patients: 1964, 911, 887, 591, 439, 363, 408, 491,
406; in the other subjects: 1191, 698, 535, 370, 338, 370, 363, 394, 401. Reprinted from
Neuroscience Letters, 235, Szelag E.v. Steinbüchel N., Pöppel E. "Temporal process-
ing disorders in patients with Broca’s aphasia" 33–36.
copyright (1997) with permission from Elsevier
deficits, because limited duration of consonants and vowels in incoming words

could not be properly decoded because of disrupted timeframe.
In contrast, Broca’s aphasic patients were unaffected on this high processing
level (Figure 12.2). They were characterized by relatively preserved compre-
hension but nonfluent speech and displayed deficits within the supra-second
processing range (Figure 12.3).
Using subjective accentuation paradigm of monotonous metronome beats,
normal healthy volunteers can integrate the information up to a maximum of
ca. 3 seconds. In this task they applied a combination of integration strategies
based on perceptual grouping of separate beats in a constant time (related
to the upper limit of temporal integration, Figure 12.3 dashed parallel lines
A reflecting integration within e.g., 1000, 2000 or 4000 s time windows) and
automatic counting up to 2, 4 or 6 s (Figure 12.3 solid lines B labelled by
numbers 2, 4 or 6). In contrast, in Broca’s aphasic patients the constant time

strategy was disrupted, but the accentuation was based predominantly on
automatic mental counting (Figure 12.3 bold dashed line C). Moreover, the
upper limit of integration in Broca’s aphasic patients exceeded the typical
frames characteristic for normal healthy volunteers. This suggests deficient
temporal integration in motor aphasic patients in a time window of a few sec-
onds, but relatively preserved automatic mental counting. The data obtained
implied that some highly structured syntactic abilities related to temporal
integration are located in the anterior language area (Broca’s area).
The evidence provided by Szelag et al. (1997) and v. Steinbüchel et al. (1999);
Table 12.2 point 10–11; Figure 12.2 and 12.3) showed that a disruption in tempo-
ral binding is a core symptom in case of nonfluent speech and agrammatism,
dominating in motor aphasia. In fact verbal expression requires information to
be integrated and held for a few seconds. The disruption of temporal integra-
tion at the level of seconds may cause symptoms typical for motor aphasia.
Furthermore, aphasic patients demonstrated impaired self-paced (per-
sonal) tempo of finger tapping, indicating the dominant control of left hemi-
sphere in voluntarily timed actions in the special time scale of hundreds of
milliseconds involved in motor behaviour (Wittmann et al., 2001; Figure 12.4).
These timing deficits may be related to disrupted TIP linked to the syllable
level, independently of the type of aphasia.
To conclude, we argue that TIP in aphasics may be selectively affected at
either sub- or supra-second time range, depending on the localisation of lesion
and observed disfluency pattern. We also postulate that a disruption of timing
mechanisms leads to phonological and/or syntactical disorders, commonly
observed in aphasic patients.
These results may have some practical applications with respect to new
neurorehabilitation methods. As TIP processing is impaired in aphasic
patients, in our recent studies we verified the effectiveness of a new method of
aphasia therapy which is concentrated not on the linguistic level, but on the
pre-semantic one and concerns the training of neuronal mechanisms underly-
ing both TIP and language (Szelag et al., 2014). These methods address both the
receptive and expressive language functions, in particular, auditory speech
comprehension, phonemic hearing and nonfluent verbal output.
Our recent studies are addressed greater understanding of the relationship
between timing and cognition (Szelag et al., 2011). Using Fast For Word
Language® (ffw) program, we showed for the first time significant benefits of
such temporal training on broad aspects of cognitive function in the elderly
beyond 65 years of life (Szelag and Skolimowska, 2012). Following such train-
ing, we indicated stable positive effects not only in TIP, but also in divided and
352 Szelag et al.
Figure 12.4 Maximum-tapping tempo and personal-tapping tempo as mean inter-response

interval (iri) over the orthopaedic control group and the brain-injured patient
groups with left-hemispheric cortical lesions (lh), with left-hemispheric lesions in
predominantly subcortical regions (lh sub) and with right-hemispheric cortical
lesions (rh). Data for the brain-injured patients are only presented for the hand
ipsilateral to the lesion site. Reprinted from Cognitive Brain Research, 10,
Wittmann M., v. Steinbüchel N., Szelag E. “Hemispheric specialisation for self-
paced motor sequences” 341–44.
copyright (2001) with permission from Elsevier
vigilance of attention, matching complex patterns, and working memory span.

These results show a new impact of temporal training not only on deficient
language function, but also on age-related cognitive decline in the senior
population.
On the basis of these results we offer a promising direction for neuroreha-
bilitation and have recently initiated an innovative rehabilitation computer
program that addresses improvement of a broad range of cognitive functions
in children and adults.
8 Concluding Remarks
Aphasia is a complex language disorder and refers to deficits apparent in

speech, writing, and reading caused by an injury to brain areas, specialized for
these functions. It is commonly known that the expression and reception
of language have defined temporal dynamics and involve highly skilled coordi-
nation of several processes. Language processing depends, thus, on the
temporal constraints of information processing which may be affected after

injury to the brain.
In this chapter we summarize the existing literature studies on TIP as a key
to understand language disturbances in aphasic syndromes. The literature
data are illustrated with examples from our studies, indicating parallel lan-
guage and timing deficits following damage to specific brain regions. We
showed dissociation between receptive and expressive language deficits asso-
ciated with a disruption of specific timing mechanisms controlling informa-
tion processing on milliseconds or multiseconds time domains.
To conclude, in aphasic patients TIP may be selectively affected either
within the sub- or supra-second range, depending on the lesion location and
observed disfluency pattern. A disruption of timing mechanisms leads to pho-
nological disorders and/or effortful nonfluent speech. Finally, we have indi-
cated that the specific nonverbal training in temporal processing can
ameliorate auditory comprehension in aphasic patients. These studies provide
an important contribution to our understanding of TIP as a neural basis of
language, as well as other cognitive function.
Acknowledgments
Supported by grants 507/1/N-DFG/2009/0 and INNOTECH/IN1/30/159041/

NCBR/12. We wish to thank Argiro Vatakis and Melissa Allman for the helpful
reading of this chapter.
References
Blanken, Gerhard et al. 1993. Linguistic Disorders and Pathologies, Berlin – New York
(Walter de Gruyter).
Efron, Robert. 1963. “Temporal Perception, Aphasia and Déjà vu” Brain 86: 403–24.
Fink, Martina, Jan Churan, and Marc Wittmann. 2006. “Temporal Processing and
Context Dependency of Phoneme Discrimination in Patients with Aphasia” Brain
and Language 98: 1–11.
Hirsh, Ira J., and Carl E. Sherrick. 1961. “Perceived Order in Different Sense Modalities”
Journal of Experimental Psychology 62: 423–32.
Kagerer, Florian A. et al. 2002. “Cortical Involvement in Temporal Reproduction:
Evidence for Differential Roles of the Hemispheres” Neuropsychologia 40(3):
357–66.
354 Szelag et al.
Kanabus, Magdalena et al. 2002. “Temporal Order Judgement for Auditory and Visual
Stimuli” Acta Neurobiologiae Experimentalis 62: 263–70.
Osterhout, Lee. 2000. “On space, time, and language: For the next century, timing is
(almost) everything” Brain and Language 71: 175–7.
Penfield, Wilder, and Lamar Roberts. 1959. Speech and Brain Mechanisms, New York:
Princeton University Press.
Pöppel, Ernst. 1997. “A Hierarchical Model of Temporal Perception” Trends in Cognitive
Sciences 1: 56–61.
———. 2004. “Lost in time: A historical frame, elementary processing units and the
3-second window” Acta Neurobiologiae Experimentalis 64: 295–302.
———. 2009. “Pre-Semantically Defined Temporal Windows for Cognitive Processing”
Philosophical transactions of the Royal Society, Series B, Biological Sciences 364:
1887–96.
Price, Cathy. 2004. “An Overview of Speech Comprehension and Production” In Human
brain function edited by Richard Frackowiak, Karl J Friston, Christopher D Frith.
Raymond J Dolan, Cathy Price, Semir Zeki, John T. Ashburner and William D Penny,
517–32. Oxford: Elsevier.
Purves, Dale et al. 2008. Principles of Cognitive Neuroscience Sunderland – Massachusetts
usa: Sinauer Assoc., Inc. Publishers.
Scott, Sophie K. 2012. “The neurobiology of speech perception and production – can
functional imaging tell us anything we did not already know?” Journal of
Communication Disorders 45: 419–25.
Sidiropoulos, Kyriakos et al. 2010. “Temporal Processing Capabilities in Repetition
Conduction Aphasia” Brain and Cognition 73(3): 194–202.
Springer, Sally P., and Georg Deutsch. 1989. Left Brain, Right Brain New York: H. Freeman
and Co.
Stefanatos, Gerry A. et al. 2007. “Fine Grain Temporal Analysis in Aphasia: Evidence
from Auditory Gap Detection” Neuropsychologia 45(5): 1127–33.
Swisher, Linda, and Ira J. Hirsh. 1972. “Brain Damage and the Ordering of Two
Temporally Successive Stimuli” Neuropsychologia 10: 137–52.
Szaflarski, Jerzy P. et al. 2011. “Poststroke Aphasia Recovery Assessed with Functional
Magnetic Resonance Imaging and a Picture Identification Task” Journal of Stroke
and Cerebrovascular Disease 20(4): 336–45.
Szelag, Elzbieta et al. 2004. “Individual Differences in Temporal Information Processing
in Humans” Acta Neurobiologiae Experimentalis 64: 349–66.
Szelag, Elzbieta et al. 2008. “Cortical Representation of Time and Timing Processes” In
Neuronal correlates of thinking, edited by Eduardo Kraft, Balazs Guylas and Ernst
Pöppel, 185–99. Berlin, Springer-Verlag.
Szelag, Elzbieta et al. 2011. “Hearing Loss and Auditory Processing Disorders: Clinical
and Experimental Perspectives” In Culture and Neural Frames of Cognition and
Communication edited by Shihui Han and Ernst Pöppel, 153–68. Berlin: Springer.
Szelag, Elzbieta et al. 2009. “Neuropsychological Rehabilitation from Brain-Behavior

Perspective” In New Ideas in Studying and Supporting Development of Exceptional
People edited by Ewa Pisula and Piotr Tomaszewski, 49–63.Warszawa: Wydawnictwo
Uniwersytetu Warszawskiego.
Szelag, Elzbieta, Nicole v Steinbüchel, and Ernst Pöppel. 1997. “Temporal Processing
Disorders in Patients with Broca’s Aphasia” Neuroscience Letters 235: 33–6.
Szelag, Elzbieta, and Justyna Skolimowska. 2012. “Cognitive Function in Elderly Can be
Ameliorated by Training in Temporal Information Processing” Restorative Neurology
and Neuroscience 30: 419–34.
Szelag, Elzbieta et al. 2014 “Training in Temporal Information Processing Ameliorates
Auditory Comprehension in Aphasic Patients: A Randomized Controlled Pilot
Study” Journal of the Neurological Sciences 338: 77–86.
Tallal, Paula, and Freda Newcombe. 1978. “Impairment of Auditory Perception and
Language Comprehension in Dysphasia” Brain and Language 5: 13–24.
Turken, And U., and Nina F. Dronkers. 2011. “The neural architecture of the language
comprehension network: converging evidence from lesion and connectivity analy-
sis” Frontiers in Systems Neuroscience 5(1): 1–20.
von Steinbüchel Nicole, Marc Wittmann, and Elzbieta Szelag. 1999a. “Temporal
Constraints of Perceiving, Generating and Integrating Information: Clinical
Evidence” Restorative Neurology and Neuroscience 14: 167–82.
von Steinbüchel Nicole, . 1999b. “Auditory Temporal-Order Judgement is Impaired in
Patients with Cortical Lesions in Posterior Regions of the Left Hemisphere”
Neuroscience Letters 264: 168–71.
Wittmann Marc et al. 2004. “Effects of Brain-Lesion Size and Location on Temporal
Order Judgement” Neuroreport 15(15): 2401–5.
Wittmann Marc Nicole v Steinbüchel, and Elzbieta Szelag. 2001. “Hemispheric
Specialisation for Self-Paced Motor Sequences” Cognitive Brain Research 10: 341–4.
Zaidel, Eran. 2001. “Hemispheric Specialization for Language in the Split Brain” In
Handbook of neuropsychology: Language and aphasia, edited by François Boller and
Jordan Grafman, 393–418. Amsterdam: Elsevier.
Zaidel, Eran et al. 2003. “The Callosal Syndromes” In Clinical Neuropsychology edited by
Kenneth M Heilman and Edward Valenstein, 347–403 (4th edition). New York:
Oxford University Press, Inc..
Zampini, Massimiliano, David I. Shore, and Charles Spence. 2003. “Audiovisual
Temporal Order Judgments” Experimental Brain Research 152(2): 198–210.
Zampini, Massimiliano et al. 2005. “Audiotactile Temporal Order Judgments” Acta
Psychologica 118(3): 277–91.

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Brill

Chapter Title: Aphasia as a Temporal Information Processing Disorder

Book Title: Time Distortions in Mind

This book is licensed under a Creative Commons Attribution-NonCommercial 4.0

Aphasia as a Temporal Information Processing

Elzbieta Szelag* ,✝, Aneta Szymaszek* ,✝, and Anna Oron*

* Laboratory of Neuropsychology, Nencki Institute of Experimental Biology, Warsaw, Poland.

© Elzbieta Szelag, Aneta Szymaszek, & Anna Oron, 2015 | doi 10.1163/9789004230699_013

In the present chapter, we concentrate on language functions, especially on

Language is a highly specialized mental function that is a key factor in social

3 Epidemiology, Definitions, and Clinical Syndromes of Aphasia

The term aphasia denotes acquired disturbances of language processing,

Type of aphasia Classic location of brain damage Particular language functions

spontaneous comprehen- repeti- naming

All use subject to https://about.jstor.org/terms

problem in modern society. This should inspire researchers worldwide to

4 The Neuroanatomical Basis of Language

Current knowledge on understanding cerebral representation of language

4.1 Clinical Observations of Language Deficits

4.2 Electrophysiological Mapping of Brain Areas

4.3 ‘Split-brain’ Studies

4.4 Experimental Studies

4.5 Summary of Cortical Regions Supporting Language

communication subcortical structures are involved, e.g., basal ganglia, insula,

Figure 12.1 The differential diagnosis of main aphasic syndromes.

No Author Subjects Method Results Conclusions

Evidence from milliseconds timing

All use subject to https://about.jstor.org/terms

to report which stimulus in the pair was to order tonal stimuli.

All use subject to https://about.jstor.org/terms

et al., 1999b. with lh damage; monaurally;

No Author Subjects Method Results Conclusions

14 fluent AP with lh Task:

All use subject to https://about.jstor.org/terms

All use subject to https://about.jstor.org/terms

cular lesion; broadband and filtered noise of different

No Author Subjects Method Results Conclusions

All use subject to https://about.jstor.org/terms

All use subject to https://about.jstor.org/terms

No Author Subjects Method Results Conclusions

All use subject to https://about.jstor.org/terms

Despite the general features of neuroanatomical basis of language described

5 Temporal Constraints of Speech

Both everyday observations and experimental data indicate temporal con-

Thus, spontaneous flow of speech is temporally segmented or ‘chunked’ in a

6 Deficits in Processing Temporal Information in Aphasic Patients

Studies of patients suffering from aphasia following left hemispheric brain

7 Relationships between Disrupted Timing and Specific Aphasia

It seems also interesting to note, that in our studies on disrupted timing in

range was assessed with auditory temporal-order-threshold (Figure 12.2

deficits, because limited duration of consonants and vowels in incoming words

numbers 2, 4 or 6). In contrast, in Broca’s aphasic patients the constant time

Figure 12.4 Maximum-tapping tempo and personal-tapping tempo as mean inter-response

vigilance of attention, matching complex patterns, and working memory span.

Aphasia is a complex language disorder and refers to deficits apparent in

temporal constraints of information processing which may be affected after

Supported by grants 507/1/N-DFG/2009/0 and INNOTECH/IN1/30/159041/

Szelag, Elzbieta et al. 2009. “Neuropsychological Rehabilitation from Brain-Behavior

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