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Aphysiological change in the homotopic cortex following left posterior temporal lobe infarction.

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ORIGINAL ARTICLES
A Physiological Change in the Homotopic
Cortex following Left Posterior Temporal
Lobe Infarction
Alexander Leff, BSc, MRCP,1 Jennifer Crinion, BSc,1 Sophie Scott, PhD,1 Federico Turkheimer, PhD,2
David Howard, PhD,3 and Richard Wise, FRCP1
We investigated the relationship between cerebral activity (measured with positron emission tomography) and word rate
in normal subjects and aphasic patients listening to monosyllabic words at rates up to those encountered in normal
speech. By measuring the slope of the regression of the individual activity–word rate responses in the temporal cortex in
normal subjects, we identified a functional asymmetry in the posterior superior temporal sulcus. The response was
greater (steeper) on the left. Using the same study design, we identified a steeper activity–word rate response in the right
posterior superior temporal sulcus of patients who had recovered single-word auditory comprehension after infarction of
the left posterior temporal cortex. This response was significantly different from that observed in both normal subjects
and a group of patients with left hemisphere infarcts that spared the posterior temporal cortex. The results demonstrated
a change in physiological responsiveness in the contralateral homotopic cortex after posterior temporal infarction.
Ann Neurol 2002;51:553–558
Over a century ago, Jackson1 suggested that recovery
from aphasic stroke depends, at least in part, on a laterality shift; that is, the cortex contralateral to the lesion takes over one or more language functions. Although this mechanism is accepted as dogma by many
aphasiologists, direct demonstrations are rare.2 It is at
least as likely in many instances that recovery is the
result of only partial damage to left hemisphere language systems, with the return of perilesional function
after the acute injury. When right hemisphere regions
do have a role, the function may have been distributed
between the two hemispheres before the stroke.
Most functional neuroimaging studies have demonstrated symmetrical increases in activity in the superior
temporal cortex in response to listening to speech or
speechlike stimuli.3–5 Only recently have more sophisticated study designs shown clearly that symmetry of
blood flow responses does not imply symmetry of
function; therefore, the symmetrical superior temporal
cortical responses, lateral and anterior to the primary
auditory cortex (PAC), in response to words contrasted
with complex noise stimuli6 can be distinguished with
an alternative acoustic stimulus for the baseline condition.7 However, a consistent region of asymmetry in a
number of studies has been the posterior superior temporal cortex, specifically in the posterior superior temporal sulcus (pSTS).6 – 8
On the basis of this observation, we designed a study
to investigate directly the possibility of a laterality shift
after left posterior temporal cortical infarction. This
study had a number of advantages. First, previous studies had strongly identified a very precise brain region to
investigate. Second, probabilistic maps for the PAC
and the planum temporale (PT) lying posterior to the
PAC in the supratemporal plane have been published;
these allowed adjustments to be made for anatomical
left–right asymmetries in the posterior superior temporal cortex. Third, we know that activation of the left
pSTS is obligatory; that is, it is observed in response to
passive perception of speech stimuli. The effects of attention or top–down modulation during the performance of metalinguistic tasks create uncertainties when
results are extrapolated from studies incorporating decisions and responses to speech stimuli to normal, implicit speech perception.9
Initially, we investigated the following hypothesis,
that activity within the left pSTS of normal subjects
would increase as a function of the rate of hearing
From the 1Medical Research Council Cyclotron Unit, Clinical Sciences Centre, Hammersmith Hospital, Imperial College School of
Medicine, London; 2Imaging Research Solutions Limited, Cyclotron
Building, Hammersmith Hospital, London; and 3Department of
Speech, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
Published online Apr 23, 2002
in Wiley InterScience
(www.interscience.wiley.com). DOI: 10.1002/ana.10181
Received Aug 3, 2001, and in revised form Jan 8, 2002. Accepted
for publication Jan 9, 2002.
Address correspondence to Dr Leff, Medical Research Council Cyclotron Unit, Clinical Sciences Centre, Hammersmith Hospital, Imperial College School of Medicine, London W12 0NN, United
Kingdom. E-mail: alexander.leff@ic.ac.uk
© 2002 Wiley-Liss, Inc.
553
words but the response within the right pSTS would
be attenuated relative to the left. As the left pSTS is
equally responsive to word lists and meaningful sentences, we used monosyllabic word lists as the stimuli.
Confirmation of this hypothesis would give us a
method for investigating aphasic stroke patients. We
predicted that, compared with normal control subjects,
stroke patients with a chronic infarct that included the
left pSTS would demonstrate an increase in the activity–word rate response of the right pSTS, whereas patients with left hemisphere infarction that spared the
pSTS would show no change in the response of the
right pSTS. This would be an indirect demonstration
of synaptic reorganization in the right pSTS in response to loss of the mirror region in the left hemisphere.
This was intended primarily as a biological, rather
than neurobehavioral, observation. A correlation of activity changes with behavioral improvements could
only be tentative, for two reasons. First, the patients
were studied only once. Second, cerebrovascular accidents lack the precision of experimental surgical lesions
in nonhuman primates, obeying vascular, not functional, boundaries. An aphasic stroke usually results in
multiple associated deficits, and we were only investigating one small region, which had been identified in
previous functional neuroimaging studies of normal
subjects and not from lesion-deficit analyses of patients. The occurrence of parallel recovery of functions
localized to damaged cortical regions adjacent to the
left pSTS would result in chance associations when behavioral measures were related to the activity–word rate
response in the right pSTS.
Subjects and Methods
Patients and Controls
Eight normal subjects (4 men, 40 – 61 years) and 15 patients
(11 men, 43–76 years) were studied. They all had English as
their first language and were right-handed. Each gave informed consent to participate in the study. The local ethics
committee approved the project, and permission to administer radioisotopes was given by the Department of Health.
Each patient also had a high-resolution magnetic resonance
imaging scan for identification of the site and size of his or
her stroke. The patients also underwent tests of their abilities
to perceive and understand speech. The patients were recruited consecutively from a special-interest aphasia clinic.
The inclusion criteria were as follows. The patients had to be
younger than 80 years of age; have had only one stroke
(based on history and magnetic resonance imaging findings,
excluding small, focal, white matter signal changes so common in the elderly); and have had no historical or clinical
evidence of any other neurological condition, such as dementia. The patients were then divided into two groups based on
whether the left pSTS was or was not included in the infarct.
554
Annals of Neurology
Vol 51
No 5
May 2002
Stimuli
All stimuli used were single-syllable English nouns and verbs
obtained from the MRC Psycholinguistics database, with the
following specifications: mean word length, 3.4 phonemes;
mean imageability, 511 (range, 353– 647); and mean log frequency, 1.5 on the Kucera and Francis scale. The stimuli
were recorded in an anechoic room by a female speaker. The
articulation rate was fast with equivalent stress. The stimuli
were digitized at 8-bit 22KHz. Only those words that were
less than or equal to 330ms in duration but easily comprehensible were processed further (n ⫽ 250). Therefore, the
duration of the words was kept fixed across all rates, the
length of the syllables being the same as those encountered in
normal, connected speech. The stimuli were presented randomly with PsyScope software.10 The inter-onset interval
was varied between 333 and 6,000ms to alter the rate of
presentation. Presentation was binaural, with the volume set
at a comfortable level by each subject. The stimuli did not
sound like continuous speech because every word (syllable)
was stressed and the inter-onset interval was fixed in any
block of stimuli. The subjects reported no difficulty perceiving the stimuli as individual words across all rates. There was
only one condition: listening to monosyllabic words at eight
different rates (10, 35, 55, 70, 85, 95, 115, and 130 words
per minute). Each word was repeated once across 16 scans,
with the scan order randomized for each subject and between
subjects. The subjects listened with their eyes closed and
were asked simply to listen to the words.
Image and Statistical Analysis
Subjects were studied with a CTI-Siemens ECAT EXACT
HR⫹⫹/966 positron emission tomography scanner (CTI,
Knoxville, TN) operated in the high-sensitivity, threedimensional mode. H215O was administered intravenously.11
SPM99 software (Statistical Parametric Mapping, Wellcome
Department of Cognitive Neurology, Institute of Neurology,
University College, London, UK) was used to realign and
spatially normalize the scans into standard Montreal Neurological Institute space.12 The Talaraich & Tournoux template13 and Montreal Neurological Institute template occupy
different spaces, so we gave coordinates for both Montreal
Neurological Institute and Talaraich & Tournoux spaces.
The patients were normalized into Montreal Neurological
Institute space with a program that used a hand-drawn mask
of the stroke (derived from the magnetic resonance imaging
scan) to prevent the normalization algorithm from defining
the edge of the infarct as part of the brain surface.14 Scans
were smoothed with an isotropic, 8mm, full-width, halfmaximum Gaussian kernel to account for variation in gyral
anatomy and to improve the signal-to-noise ratio. The normal subjects were initially entered alone into a design matrix
to investigate left temporal lobe responses (first analysis).
When comparing the data from the patients with left hemisphere infarction and from the normal controls, we could
only investigate voxels common to all subjects; therefore, no
data were available from most of the left temporal lobe (second analysis). Each subject was entered as a separate study
into a multigroup design matrix with word rate as the covariate of interest, which permitted the statistical map for
each individual to be evaluated. Therefore, the statistical
parametric maps were of the significance, converted to
Z-scores, of the correlation coefficients for each voxel. The
first and second analyses both included a blocked analysis of
covariance with global counts as confounds, to remove the
effects of global changes in perfusion across scans. Scan order
was entered as a subject-specific covariate of no interest to
control for nonspecific time effects. In the grouped analyses,
the threshold for the significance of a change in activity in
the peak voxel of an activated region was set at p ⬍ 0.05
corrected for analyses across the whole volume of the brain.
Anatomical Considerations and Analysis of Data
Outside Statistical Parametric Mapping
There are anatomical and functional asymmetries in the human temporal lobe, so we used probabilistic maps to identify
left and right PAC and PT,15,16 defining the pSTS as lying
in the superior temporal cortex posterior to the PAC and
ventral and lateral to the PT.
The statistical parametric mapping design matrix identified voxels with high correlation coefficients for a positive
relationship between word rate and regional cerebral blood
flow. We also wished to investigate the steepness of this relationship from the slope of the regression. For each subject,
the peak voxel was identified in bilateral pSTS (first level,
first analysis) or right pSTS (first level, second analysis) with
the anatomical probabilistic maps. Regional cerebral blood
flow data from these peaks were plotted. The slopes of the
regressions were calculated and entered into a second-level
analysis in a one-tailed, paired t test (second level, first analysis) or a two-group, unpaired t test (second level, second
analysis).
Results
First Analysis
There were two distinct peaks in the superior temporal
gyrus of both hemispheres that were paired in terms of
both location and activity–word rate response (Fig 1).
The first pair had a high (75–100%) probability of being located in PAC,15 with no significant difference in
the slopes of the regressions between hemispheres ( p ⫽
0.8: left ⫽ 0.17, right ⫽ 0.16). The other pair was
located about 10mm laterally and anteriorly to PAC in
the lateral superior temporal gyrus. Again, there was no
asymmetry between hemispheres ( p ⫽ 0.3: left ⫽
0.14, right ⫽ 0.15). In addition, there were subpeaks
that localized to the left and right PT. There was a
separate peak in the left pSTS that was not paired with
a mirror voxel in the right hemisphere (see Fig 1) at
the conservative threshold set for significance. This
peak (coordinates: ⫺60 ⫺36 4, [⫺59 ⫺35 5]; p ⬍
0.001, corrected) was posterior to PAC15 and ventrolateral to the PT.16 The peak voxel in the homotopic
cortex was identified only when the statistical threshold
was reduced (coordinates: 62 ⫺32 ⫺2, [61 ⫺31 0];
p ⬎ 0.9, corrected). When the left and right pSTS
peaks were identified from the individual analysis for
each subject, a paired t test showed a significant difference between hemispheres in the slopes of the regres-
sions ( p ⬍ 0.05). The average difference between
slopes was 0.03. Although a statistical analysis was not
performed on the mean slopes of the regressions for
each side, these were left ⫽ 0.13 and right ⫽ 0.10.
Second Analysis
The patients were divided into two groups based on
the sites of their lesions. A neurologist who was unaware of the functional neuroimaging results determined from sagittal, coronal, and axial views of the anatomical magnetic resonance imaging scans whether
the left pSTS was or was not included in the infarct.
When the activity–word rate responses in the right
hemispheres of the patients with left pSTS infarction
(pSTS⫹) were compared with the activity–word rate
responses in the normal controls and the patients without left pSTS infarction (pSTS⫺), a significant response in the right pSTS was identified only in the
pSTS⫹ patient group (coordinates: 62 ⫺36 2, [61
⫺36 4]; p ⬍ 0.001, corrected; Fig 2). The peak voxel
within the right pSTS was identified from each subject’s individual analysis and the slope of the regression
determined. A one-tailed, two-group t test comparing
the slopes of the regressions from the pSTS⫹ patient
group with those from the combined results for the
normal controls and the pSTS⫺ patient group showed
a significant difference ( p ⬍ 0.05; see Fig 2).
Behavioral Data and Infarct Size
All 6 patients with damage to the left pSTS had documented evidence in their case notes of, among other
language deficits, a marked deficit in single-word comprehension in the acute stage of their strokes. All had
been assessed by an experienced speech and language
therapist with a range of different standardized test batteries. Five patients from the pSTS⫹ group and all 9
patients from the pSTS⫺ group were tested on a range
of behavioral tests within 6 weeks of their positron
emission tomography scans. One died (of complications following a fractured hip) soon after his positron
emission tomography scan and before behavioral testing was completed. Unless stated otherwise, comparisons between the test results from the two groups were
nonparametric Mann-Whitney U tests. No Bonferroni
correction was applied. The results are presented as a
ratio of mean pSTS⫹ patients to mean pSTS⫺ patients, with p values.
There was no difference between the two groups in
age (61 [range, 50 –75]:59 [range, 43–73] years, p ⫽
0.3), time between infarct and testing (31 [range,
6 –76]:28 [range, 5–70] months, p ⫽ 0.7), or infarct
size (7 [range, 0.5–14]:3 [range, 0.5–10] percent of total brain volume [interquartile range: 13:3], p ⫽ 0.3).
The groups were also matched on a number of psychological tests: nonverbal reasoning, with Ravens Coloured Progressive Matrixes17 (9:10, p ⫽ 0.3); semantic
Leff et al: Change in the Homotopic Cortex
555
Fig 1. The group activations for the 8 normal subjects who listened to single words at
increasing rates were projected onto the T1
Montreal Neurological Institute template in
axial (left, z ⫽ 4) and coronal (right, y ⫽
⫺36) sections. Two paired peaks are seen in
the primary auditory cortex (PAC) and lateral superior temporal gyrus (1 and 2, respectively); a third, unpaired peak is seen
posterior and ventral to the PAC on the left
in the posterior superior temporal sulcus
(PSTS; 3). Below, activity–word rate curves
are shown for the 8 normal subjects (a–h).
Data were plotted out from the peak voxel
in the left (filled squares) and right (open
circles) pSTS from their own individual
statistical parametric maps {t} (not shown),
with the activity (percentage signal change),
against the eight word rates. Each point is
an average of the two repetitions at each
rate. Linear fits are shown in solid (left)
and dashed (right) lines. % ⫽ percentage of
signal change; wpm ⫽ words per minute.
Fig 2. The regional cerebral blood flow response to the increasing
word rate in the 6 patients with left posterior superior temporal
sulcus (pSTS) infarction (pSTS⫹) is shown, masked by activity
from both the 8 normal subjects and the 9 control patients without left PSTS infarction (pSTS⫺); the peak is in the right pSTS.
Activity was projected onto the mean normalized T1 magnetic
resonance imaging of the 6 pSTS⫹ patients in axial (left, z ⫽
2) and coronal (right, y ⫽ ⫺36) sections. Below is a plot of the
average regression coefficient (R) for the three groups, consisting of
data extracted from their own individual statistical parametric
maps (not shown). The table displays the mean (R) and standard
error (SE) of each of these values. pSTS⫹ patients had significantly steeper activity rate responses in the right pSTS than both
the normal subjects and the pSTS⫺ patients.
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Annals of Neurology
Vol 51
No 5
May 2002
decisions, with 10 items from the Dutch Pyramids and
Palm Trees test18 (9:10, p ⫽ 0.6); visual recognition
memory (9:10, p ⫽ 0.9); the British Picture Vocabulary Scale,19 aural (71:73, p ⫽ 0.7) and written (67:73,
p ⫽ 0.4); and the Action for Dysphasic Adults lexical
decision battery,20 aural (7:7, p ⫽ 0.9), and written
(7:7, p ⫽ 0.8). The only test on which the pSTS⫹
patients performed worse than the pSTS⫺ patients was
auditory maximal pairs21 (42:45, p ⫽ 0.04), an offline
phoneme discrimination test (eg, dis and dis, sut and
dut, with a same/different judgment on the pairs).
Discussion
The use of functional neuroimaging to demonstrate a
laterality shift in response to speech perception following an aphasic stroke is dependent on a study design
that can demonstrate a robust asymmetry in normal
subjects. This has proven difficult to do because speech
is a complex acoustic signal containing more than just
phonetic and lexical information. Therefore, it is important to distinguish between perception of speech
and perception of phonemic and lexical information in
the speech signal.5,7,14 Like other neuroimaging studies
that used a parametric design involving the hearing of
words at an increasing rate, our study demonstrated
that the responsiveness of the PAC and the temporal
cortex anterior and lateral to the PAC was symmetrical.
Equal responsiveness does not imply similar processing
functions, and a recent study has made a clear functional distinction between the left and right anterolateral temporal cortex on the basis of contrasts between
carefully controlled speech and nonspeech stimuli.7
However, this study demonstrated that, in normal subjects, the left pSTS had a greater response to hearing
monosyllabic nouns of uniform duration at increasing
rates than the right pSTS. This accords with an asymmetry of the identical region demonstrated in other
functional neuroimaging studies, including those that
have contrasted the response to acoustically different
stimuli.
This study used a baseline of listening to words at a
slow rate rather than rest. A further and probably critical difference in the design was that it kept the duration of each word the same across all rates. To our
knowledge, previous studies did not correct for the
confounders of word rate and duration; when the stimuli were prepared, the speaker had to shorten the duration of words (mainly by shortening the lengths of
vowel sounds) when reading the word lists at the faster
rates. In our study, syllables were of constant durations
encountered in everyday connected speech. Therefore,
this study identified a lateralized auditory system with
the capacity to respond incrementally up to the rate of
hearing words encountered in normal speech.
Having established an asymmetrical response in the
pSTS of normal subjects, we went on to demonstrate
that in a group of right-handed patients with strokes
affecting their left pSTS, the mean activity rate response in the right pSTS was the same as that observed
in the left pSTS of the normal subjects and significantly steeper than the right pSTS response both in
normal subjects and in patients with left hemisphere
infarction that spared the left pSTS. This result indirectly confirms synaptic reorganization, indexed by a
change in physiological response, in the homotopic
cortex of these patients.
Several studies have used functional imaging to investigate stroke recovery and the role, if any, that a
laterality shift plays in recovery. Our data differ from
these studies in three ways. First, we correlated changes
in regional cerebral activity with implicit speech perception, avoiding the confounder of differences in performance between normal controls and patients when
using explicit tasks to test functional brain systems.22–26 Second, we used a more rigorous methodology than was used in other studies23,26,27 for spatial
normalization and referred to anatomical probabilistic
maps to ensure that we were comparing, as far as possible, the same anatomical region between groups. Importantly, we performed the critical statistical tests on
the data from individual subject analyses, which acknowledged intersubject anatomical differences in the
posterior temporal cortex. Third, we used a random
effects statistical model when comparing the data between subject groups, making the demonstration of a
functional difference in the right pSTS between groups
a more robust observation.28
In conclusion, we have demonstrated a change in the
function of the right pSTS in response to a chronic
lesion in the left pSTS, one that is not observed in
patients with chronic lesions elsewhere in the left hemisphere. This result cannot be extrapolated to other superior temporal cortical regions; alternative study designs that strongly indicate asymmetry elsewhere in
superior temporal cortex in normal controls will be required.
Previous functional neuroimaging studies have differed in their conclusions about the presence23,27,29 or
absence24,25,30 of evidence for a permanent laterality
shift after aphasic stroke, but this may simply reflect
the capacity of different local systems to relocate to the
contralateral hemisphere. What is not evident from our
study is the precise role of the left pSTS in speech perception in normal subjects, a role that plausibly was
adopted by the right pSTS in our patient group. A
recent functional imaging study speculated that the left
pSTS holds the temporal ordering of sounds within
words briefly in memory and makes these sequences
available for rehearsal (ie, repeating).8 Clinical studies31
have demonstrated that patients with damage that includes the posterior superior temporal cortex often recover single-word comprehension, as was the case in
Leff et al: Change in the Homotopic Cortex
557
our patients with pSTS damage. However, associated
recovery in functional systems adjacent to the left
pSTS may account for, or at least may have contributed to, this recovery. The perfect lesion, restricted in
size and confined to the cortex without damage to underlying white matter tracts, of a kind used in experimental studies on nonhuman primates, will almost
never occur in human cerebrovascular disease, and relating functional imaging correlates to behavioral observations on recovery will need to be circumspect.
Nevertheless, the converging evidence from a number
of functional neuroimaging studies of a role for the left
pSTS in word perception, and the similar performances on tests of single-word comprehension by patients both with and without left pSTS infarction in
this study, support the hypothesis that a laterality shift
of function between the left and right pSTS contributes to recovery of word comprehension in patients
with left posterior temporal infarction.
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