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Journal homepage: www.elsevier.com/locate/cortex

Special issue: Clinical neuroanatomy

Neurological and neuropsychological characteristics of


occipital, occipito-temporal and occipito-parietal infarction

Antje Kraft a,*, Cathleen Grimsen b, Stefanie Kehrer a, Markus Bahnemann a,


Karoline Spang b, Maren Prass b, Kerstin Irlbacher a, Martin Köhnlein a, Anika Lipfert a,
Freimuth Brunner c, Andreas Kastrup c, Manfred Fahle b,d and Stephan A. Brandt a
a
Department of Neurology, Charité Universitätsmedizin Berlin, Berlin, Germany
b
Department of Human Neurobiology, University of Bremen, Bremen, Germany
c
Medical Hospital Gesundheit Nord, Klinikum Bremen Mitte, Bremen, Germany
d
The Henry Wellcome Laboratories of Vision Sciences, City University London, London, UK

article info abstract

Article history: Neuropsychological deficits after occipital infarction are most often described in case
Received 23 November 2011 studies and only a small sample of studies has attempted to exactly correlate the
Reviewed 16 February 2012 anatomical localization of lesions with associated neuropsychological symptoms. The
Revised 1 June 2012 present study investigated a large number of patients (N ¼ 128) in order to provide an
Accepted 15 October 2012 overview of neurological and neuropsychological deficits after occipital, occipito-
Published online xxx temporal and occipito-parietal infarction. A particular approach of the study was to
define exact anatomical correlates of neuropsychological dysfunction by using voxel-
Keywords: based lesion-symptom mapping (VLSM) in 61 patients. In addition to a visual field
Infarct topography defect and phosphenes, patients often reported anomia, difficulties in reading and
Lesion-symptom mapping memory deficits. Visual disorders, such as achromatopsia, akinetopsia or prosopagnosia,
Stroke were rarely reported by the patients. Memory and visual disorders were diagnosed
Vision efficiently using simple clinical screening tests, such as the ReyeOsterrieth Complex
Figure Test for immediate recall, the Demtect and the Lang Stereo Test. Visual field
defects, reading disorders and the perception of phosphenes were associated primarily
with lesions of the calcarine sulcus. Anomia and memory deficits were related to lesions
of the occipital inferior gyrus, the lingual gyrus and hippocampus, as well as to lesions of
principal white matter tracts.
ª 2012 Elsevier Srl. All rights reserved.

1. Introduction et al., 1999; Ntaios et al., 2011). However, several studies


have shown that occipital, occipito-temporal and occipito-
In the clinical context, occipital infarction is often perceived parietal infarction lead to additional clinical and neuro-
as being associated with visual field defects only (see Brandt psychological symptoms, such as deficits in reading, writing,
et al., 2000 for a review; Steinke et al., 1997; Yamamoto memory and executive function (Cals et al., 2002; Kumral

* Corresponding author. Department of Neurology, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.
E-mail address: antje.kraft@charite.de (A. Kraft).
0010-9452/$ e see front matter ª 2012 Elsevier Srl. All rights reserved.
http://dx.doi.org/10.1016/j.cortex.2012.10.004

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
2 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

et al., 2004; Pessin et al., 1987; Gloning et al., 1966; Maulaz the VLSM approach in a large sample of stroke patients which
et al., 2005). tries to exactly correlate a broad array of neuropsychological
Visual disorders after cerebral lesions in the occipital, deficits with anatomical lesions after occipital, occipito-
occipito-temporal or occipito-parietal cortex were described temporal or occipito-parietal infarction.
carefully in several studies in large samples of patients (e.g., The aim of the present study was to realize both: (a)
Zihl and von Cramon, 1986; Gloning et al., 1966; Rowe et al., a systematic description of subacute clinical and neuro-
2009). These studies did not distinguish between distinct psychological deficits after occipital, occipito-temporal and
etiologies such as stroke, tumors, craniocerebral injury or occipito-parietal infarction in a large sample of patients; and
hemorrhage. Notably, they did not seek to relate the exact (b) an exact clinico-anatomical correlation for these deficits
anatomical localization of lesions to associated clinical or using a VLSM approach (Rorden et al., 2007).
neuropsychological symptoms in a systematic manner. This
attempt was made by more recent reviews (e.g., Girkin and
Miller, 2001; ffytche et al., 2010) that tried to allocate certain
2. Methods
visual syndromes to specific cortical visual areas or to
a disconnection between them. But these reviews still did not
2.1. Patients
differentiate between distinct brain lesion etiologies.
Focusing on stroke, there is a limited number of reports
An overall number of N ¼ 128 patients participated in this
which give systematic overviews of neuropsychological defi-
study. Patients were recruited between 2007 and 2011 at the
cits after occipital, occipito-temporal and occipito-parietal
Department of Neurology, Charité Universitätsmedizin Berlin
infarction (Cals et al., 2002; Kumral et al., 2004; Pessin et al.,
(Berlin, Germany) and at the Stroke Unit of the Medical
1987; Gloning et al., 1966). Some larger sample studies esti-
Hospital Gesundheit Nord Klinikum Bremen-Mitte (Bremen,
mated a frequency of neuropsychological deficits such as
Germany). After receiving the approval of the local ethics
visual agnosia, dyslexia, dysphasia or memory impairment
committees, written informed consent was obtained from all
between 32% and 50% of these patients (Cals et al., 2002;
patients and the examination was conducted in conformity
Milandre et al., 1994; Steinke et al., 1997). However, these
with the Declaration of Helsinki.
studies did not allocate visual deficits or neuropsychological
Patients with ischemic cerebral infarction, as evidenced by
symptoms to specific anatomical locations within the infarct
magnetic resonance imaging (MRI) or computer tomography
territory. Such an approach was taken by numerous single
(CT), affecting the occipital gyri and sulci were included in this
case reports or small sample accounts describing neuro-
study. Apart from this primary criterion, lesions additionally
psychological deficits after posterior strokes (Pessin et al.,
extending into the temporal and/or parietal gyri and sulci were
1987; Holt and Anderson, 2000), applying the mini-mental
included as well. Both lesions involving the territories of the
state examination (Park et al., 2009), or focusing on disorders
middle cerebral artery (MCA) or posterior cerebral artery (PCA)
of reading and writing (Pillon et al., 1987; Habekost and
qualified for inclusion, if the above stated criteria were fulfilled.
Starrfelt, 2006; Pflugshaupt et al., 2009), memory (Benson
Exclusion criteria were severe aphasia, ophthalmological
et al., 1974; von Cramon et al., 1988; Machner et al., 2009),
disorders such as glaucoma, cataract or macula degeneration in
executive functions (Park et al., 2011), neglect (Park et al., 2006;
an advanced stage, or any other severe neurological or
Tomaiuolo et al., 2010) or on specific visual disorders such as
psychiatric disorder (e.g., epilepsy or schizophrenia).
visual hallucinations (Baier et al., 2010a; Tombini et al., 2012)
and visual agnosia (Landis et al., 1986; Carlesimo et al., 1998;
Ohtake et al., 2001; Konen et al., 2011). In summary, these case 2.2. Neurological testing and neuro-ophthalmological
reports offer a good overview about the diversity of visual and testing
neuropsychological deficits after occipital, occipito-temporal
or occipito-parietal infarction, but cannot contribute to Patients underwent a clinical neurological examination
a statistically valid clinico-anatomical correlation between including finger perimetry, oculomotor function, reaching,
neuropsychological deficits and anatomical areas within the motor function, extinction, neglect and reading. The basic
occipito-temporo-parietal region. neurological examination was carried out at least 24 h after
Conversely, there is only a small sample of studies that a patient received a stroke.
attempt to exactly correlate the anatomical localization of Visual acuity (near and far, using Landolt rings) and static
stroke lesions with associated clinical symptoms using perimetry (30 ) were conducted for the ipsilesional and con-
a relatively new method called “voxel-based lesion-symptom tralesional eye. The Ishihara Test of color vision (Ishihara,
mapping” (VLSM, e.g., Karnath et al., 2004). The emphasis of 1917) and the Lang Test of stereo vision (Lang, 1982) were
these studies was not to give a systematic overview about performed binocularly.
neuropsychological deficits. Instead, they focused on single In addition, patients were asked if they experienced the
clinical aspects, such as phosphenes and complex hallucina- following subjective general or visual impairments after
tions (Baier et al., 2010a), motion processing (Billino et al., stroke. General subjective impairments: 1. memory deficits, 2.
2011), neglect (Karnath et al., 2004, 2011; Bird et al., 2006; anomia, and 3. reading disorders. Specific visual subjective
Molenberghs and Sale, 2011), extinction (Chechlacz et al., in impairments: 1. visual field defects, 2. spatial orienting
press), dyslexia (Ptak et al., 2012), alexia (Pflugshaupt et al., disorder, 3. disorder of eye-hand-coordination, 4. dysfunction
2009), picture naming (Baldo et al., in press) or action recog- in visual motion perception, 5. dysfunction of recognizing
nition (Kalénine et al., 2010). To date there is no study using faces, 6. dysfunction of color vision, 7. dysfunction of stereo

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 3

perception, 8. presence of phosphenes, and 9. presence of slices, flip angle 90 , TR/TE ¼ 8000/72 msec, slice thickness
complex hallucinations. 5 mm, spacing 6 mm). For a minority of patients an additional
T1-weighted 3D image (Berlin: MPRAGE; flip angle 15 , TR/TE
2.3. Neuropsychological testing 2280/3.93 msec, voxel-size 1  1  1 mm) was acquired.
One neurologist, who was blind to the clinical symptoms
Neuropsychological testing included attention/neglect tests and the outcome of the neurological and neuropsychological
(line bisection, cancellation test, clock drawing, covert shift of assessments, classified the lesions with respect to the
attention [Posner paradigm; a subtest of the Testbatterie zur anatomical characteristics and manually delineated the
Aufmerksamkeitsprüfung (TAP) by Zimmermann and Fimm lesions to axial MRI images using MRICron software (http://
(1993)]), the Fragmented Picture Test (FPT) (Kessler et al., www.sph.sc.edu/comd/rorden/mricron/install.html) for
1993), a visual perception test [copy of the ReyeOsterrieth lesion-symptom mapping.
Complex Figure Test (ROCF, see Shin et al., 2006 for an over- Lesion classification was performed as a two-stage process:
view)], a visual/non-verbal working memory test (immediate First, it was rated, (a) whether the lesion was located in the
recall ROCF, Demtect) and a memory (Demtect delayed recall) right or left hemisphere (unilateral) or whether it was found
and dementia test (Demtect; Kalbe et al., 2004). The patient’s bilaterally; (b) whether the MCA or PCA territories were
performance in all standard neuropsychological tests was affected; (c) whether the lesion was located above or below the
assessed in relation to the performance of a normative calcarine sulcus or both; (d) whether the lesion involved
sample. lateral, medial or both aspects of the occipital cortex; and (e)
whether the lesion involved the occipital, occipito-temporal,
2.4. Image acquisition, classification of lesions and occipito-parietal or occipito-parieto-temporal cortex. For this
further lesion analysis purpose, lesions were classified using the automated
anatomical labeling (AAL) atlas of the MRICron software
Patients generally received MRI scans of the brain (only three package, which allows for identification of all major gyri. If
patients with a CT scan) with routine clinical parameters while lesions affected one of the occipital gyri, they were termed as
in the neurology service (Bremen: 1.5 T Espree, Siemens; Berlin: “occipital”. If, in addition to these, temporal gyri were
1.5 T Avanto, Siemens or 1.5 T Signa EXCITE, GE). These scans affected, they were termed as “occipito-temporal”. Likewise, if
included a T2 weighted image (Bremen: 24 slices, flip angle beyond the first, parietal gyri were also affected, they were
150 , TR/TE ¼ 8510/136 msec, slice thickness 5 mm, spacing termed as “occipito-parietal”. Lesions comprising affected gyri
6 mm; Berlin: 23 slices, flip angle 150 , TR/TE ¼ 4500/97 msec, of all three lobes were termed as “occipito-temporo-parietal”.
slice thickness 5 mm, spacing 6.5 mm or 24 slices, flip angle Second, lesions were classified according to whether or not
90 , TR/TE ¼ 5220/93 msec, slice thickness 5 mm, spacing the following anatomical regions were affected: optic radia-
6 mm), and usually also a Diffusion-weighted image (Bremen: tion, white matter, splenium, basal ganglia, mesencephalon,
24 slices, flip angle 90 , TR/TE ¼ 4400/109 msec, slice thickness thalamus, cerebellum, frontal cortex, insula and hippo-
5 mm, spacing 6 mm; Berlin: 24 slices, flip angle 90 , TR/ campus. At this step, white matter damage refers to the
TE ¼ 3500/94 msec, slice thickness 5 mm, spacing 6.5 mm or 48 subcortical white matter in general. Decisions on the lesion of

Table 1 e Descriptives.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 128 61 27 29
Age in years
Mean  SD 61.5  13.1 56.4  14.2 54.5  16.1 58.0  11.8
Range 20e85 20e82 20e73 29e77
Gender
Male 78 60.9% 38 62.3% 16 59.3% 19 65.5%
Female 50 39.1% 23 37.7% 11 40.7% 10 34.5%
Education 13.3  3.1 13.3  2.9 13.9  3.3 13.3  2.4
9e21 9e21 9e21 9e18
Handiness
Right 118 92.1% 57 93.4% 26 96.3% 26 89.7%
Left 2 01.6% 2 03.3% 0 0% 2 06.9%
Ambidexter 5 03.9% 1 01.6% 0 0% 1 03.4%
Missing 3 02.4% 1 01.6% 1 3.7% 0 0%
Time since lesion
1e10 days 102 79.7% 44 72.1% 18 66.7% 23 79.3%
11e30 days 8 06.3% 7 11.5% 3 11.1% 3 10.3%
31e150 days 5 03.9% 3 04.9% 2 07.4% 1 03.4%
150 days 13 10.2% 7 11.5% 4 14.8% 2 05.9%

Descriptive data from all patients (column 1), from all patients with a delineated lesion (column 2) and for all patients with left-hemispheric or
right-hemispheric delineated lesions (column 3 and column 4, respectively).

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
4 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

Fig. 1 e Lesion topography. Overlay of left- (upper panel) and right-hemispheric (lower panel) lesions, respectively. Note that
left-hemispheric lesions are flipped to the right side.

the optic radiation were based on a visual comparison with orientation of clinical data sets. Patients with severe atrophy,
a histological atlas (Bürgel et al., 2006). A detailed analysis of severe white matter lesions (Wahlund score > 4; Wahlund
the lesion of particular white matter tracts was performed for et al., 2001) or multiple cerebral and subcortical lesions were
VLSM results below. excluded from lesion delineation and further lesion analyses.
The patients’ T2 weighted images generally served as the An overall of N ¼ 61 patients fulfilled the criteria (31 patients
basis for lesion delineation because they offered the best were excluded due to severe white matter lesions, 18 patients
contrast for subacute brain lesions. There were only three were excluded due to severe atrophy and 19 patients were
patients, for whom an MRI scan could not be performed, excluded due to multiple cerebral and subcortical lesions).
necessitating the use of CT scans. With respect to our 24 slices For a detailed analysis of the relationship between lesions
T2 weighted images, lesions were manually drawn on 24 slices and symptoms in our group of patients, we chose a VLSM
(6 mm spacing) of a T1-weighted template MRI scan from the approach using the MRICron Software package (Rorden et al.,
Montreal Neurological Institute (MNI), thus resulting in 2007) for those neurological and neuropsychological deficits
multilayer regions of interest (ROI). Our template was slightly that were present in a relevant number of patients (10). In
rotated (pitch 8, Nudge X 1, Y 4, Z 4) to achieve the this case, Liebermeister tests as implemented in the MRICron
anterior commissureeposterior commissure (ACePC) toolset were performed to assess the statistical significance of

Table 2 e Lesion characteristics and lesion topography.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 128 61 27 29
Imaging
cMRT 116 90.6% 58 95.1% 26 96.3% 27 93.1%
cCT 12 09.4% 3 04.9% 1 03.7% 2 06.9%
Territory
PCA 106 82.8% 48 75.4% 24 88.9% 19 65.5%
MCA 17 13.3% 11 20.3% 3 11.1% 8 27.6%
Junction 4 03.1% 2 02.9% 0 0% 2 06.9%
Missing 1 .8% 0 0% 0 0% 0 0%
Wahlund score
Mean  SD 3.6  3.0 2  1.3 2  1.4 2  1.3
Range 0e13 0e4 0e4 0e4
Lobule
Occipital 47 36.7% 24 39.3% 10 37.0% 12 41.4%
Occipital-temporal 43 33.6% 20 32.8% 14 51.9% 6 20.7%
Occipital-parietal 8 06.3% 3 04.9% 0 0% 2 06.9%
Occi-pari-tempo 30 23.4% 14 23.0% 3 11.1% 9 31.0%
Relation calcarina
Above 14 10.9% 7 11.5% 3 11.1% 3 10.3%
Below 41 32.0% 19 31.1% 13 48.1% 6 20.7%
Both 72 56.3% 35 57.4% 11 40.7% 20 69.0%
Not assessable 1 .8% 0 0% 0 0% 0 0%
Position
More medial 67 52.3% 33 54.1% 18 66.7% 13 44.8%
More lateral 25 19.5% 14 23.0% 3 11.1% 11 37.9%
Both 36 28.2% 14 23.0% 6 22.2% 5 17.2%

Lesion characteristics of all patients (column 1), of all patients with a delineated lesion (column 2) and of all patients with left-hemispheric or
right-hemispheric delineated lesions (column 3 and column 4, respectively).

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 5

the lesion-symptom-mappings (Rorden et al., 2007). For phase (1e10 days) after infarction. There were no significant
precise clinico-anatomical correlations, statistical results group differences in age, gender distribution, or years of
were mapped to atlases of gyral structures and Brodmann formal education for patients with left-hemispheric delin-
areas (BAs) as implemented in MRICron, as well as to white eated lesions versus those with right-hemispheric delineated
matter tracts using a diffusion tensor imaging-based atlas lesions.
developed by Thiebaut de Schotten et al. (2011). If a particular
deficit was present in less than 10 patients, we refrained from 3.2. Anatomy and infarct topography
a detailed statistical analysis. Instead, the lesion topography
was illustrated using the subtraction analysis tool of MRICron, The lesion topography is illustrated in Fig. 1 and the lesion
which displays the overlap of lesions of patients with characteristics are further detailed in Table 2. In most cases
a particular deficit versus those lesions of patients without the infarction was located in the PCA territory. The center of
this deficit (see Karnath et al., 2002). mass of lesions for the whole group was located medially in
the occipito-temporal cortex. Left-hemispheric lesions in
patients were most often located medially in the occipito-
3. Results temporal cortex, while right-hemispheric lesions extended
more often to the occipito-parietal regions.
3.1. Descriptive Table 3 summarizes which anatomical regions were
damaged. In most patients, the optical radiation and the white
The descriptive data are summarized in Table 1. The matter were affected. Remarkably, the hippocampus was
majority of patients were investigated in the (sub-)acute affected in half of the patients with a left-hemispheric lesion.

Table 3 e Anatomical classification.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 128 61 27 29
Optic radiation
Damaged 115 89.8% 52 85.2% 24 88.9% 23 79.3%
Not damaged 13 10.2% 9 14.8% 3 11.1% 6 20.7%
White matter
Damaged 125 97.7% 60 98.4% 26 96.3% 28 96.6%
Not damaged 3 02.3% 1 01.6% 1 03.7% 1 03.4%
Splenium
Damaged 12 09.4% 6 09.8% 3 11.1% 3 10.3%
Not damaged 115 89.8% 55 90.2% 24 88.9% 26 89.7%
Not assessable 1 .8% 0 0% 0 0% 0 0%
Basal ganglia
Damaged 12 09.4% 2 03.3% 1 03.7% 1 03.4%
Not damaged 115 89.8% 59 96.7% 26 96.3% 28 96.6%
Not assessable 1 .8% 0 0% 0 0% 0 0%
Mesencephalon
Damaged 10 07.8% 3 04.9% 2 07.4% 1 03.4%
Not damaged 84 65.7% 55 90.2% 24 88.9% 28 96.6%
Missing/n.a. 34 26.5% 3 04.9% 1 03.7% 0 0%
Thalamus
Damaged 41 32.0% 15 24.6% 7 25.9% 7 24.1%
Not damaged 85 66.4% 45 73.8% 19 70.4% 22 75.9%
Not assessable 2 01.6% 1 01.6% 1 03.7% 0 0%
Cerebellum
Damaged 27 21.1% 12 19.7% 6 22.2% 3 10.3%
Not damaged 101 78.9% 49 80.3% 21 77.8% 26 89.7%
Frontal
Damaged 17 13.3% 7 11.5% 1 03.7% 6 20.7%
Not damaged 110 85.9% 54 88.5% 26 96.3% 23 79.3%
Not assessable 1 .8% 0 0% 0 0% 0 0%
Insula
Damaged 10 07.8% 2 03.3% 0 0% 2 06.9%
Not damaged 117 91.4% 59 96.7% 27 100.0% 27 93.1%
Not assessable 1 .8% 0 0% 0 0% 0 0%
Hippocampus
Damaged 48 37.5% 26 42.6% 16 59.3% 8 27.6%
Not damaged 79 61.7% 35 57.4% 11 40.7% 21 72.4%
Not assessable 1 .8% 0 0% 0 0% 0 0%

Anatomical classification all patients (column 1), of all patients with a delineated lesion (column 2) and of all patients with left-hemispheric or
right-hemispheric delineated lesions (column 3 and column 4, respectively).

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
6 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

3.3. Neurological and neuro-ophthalmological defect was subjectively declared by half of all patients. Phos-
symptoms phenes were reported in one-third of all patients.
Fig. 2 illustrates the results of statistical voxelwise lesion-
The results of the basic neurological examination are behavior mapping analyses for subjective impairments as
summarized in Table 4. Initial symptoms are shown in reported by the patients. Supplementary Fig. 1 shows the
decreasing order of frequency. While a visual deficit was re- relation of these results to important white matter tracts.
ported by the majority of patients, all other symptoms were Memory deficits were associated with lesions of the lingual
named considerably less frequently. Apart from the visual and occipital inferior gyrus, as well as the hippocampus (BA
field defect, almost no basic neurological screening test 19, 20 and 35) and lesions of the inferior fronto-occipital
applied at least 24 h after stroke revealed deficits in patients fasciculus (IFOF), inferior longitudinal fasciculus (ILF) and
with occipital infarction. the cingulum (to a minimal extent), respectively. Anomia was
Table 5 illustrates the relevant subjective impairments of correlated with inferior occipital lesions (BA 19). Reading
patients. Anomia was reported significantly more frequently disorders were associated with a lesion of the calcarine sulcus
in patients with left-hemispheric lesions (p < .05, Chi-Square- (BA 17) and lesions of the corpus callosum, as well as the IFOF
Test). There was no significant difference in the report of and ILF to a minimal extent. Visual field defects were corre-
memory deficits and reading disorder between left- and right- lated with lesions of the calcarine sulcus (BA 17) and lesions of
hemispheric groups (p > .05, Chi-Square-Test). A visual field BA 18, 19, as well as the corpus callosum. Similarly,

Table 4 e Basic neurological examination.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 128 61 27 29
Initial symptoms
Visual 102 79.7% 48 78.7% 25 92.6% 21 72.4%
Sensory 39 30.5% 20 32.8% 10 37.0% 10 34.5%
Headache 38 29.7% 24 39.4% 14 29.6% 10 34.5%
Dizziness 32 25.0% 17 27.9% 10 37.0% 4 13.8%
Paresis 20 15.6% 11 18.0% 2 07.4% 9 31.0%
Aphasia/language 18 14.1% 7 11.5% 3 11.1% 4 13.8%
Nausea/vomiting 15 11.7% 6 09.8% 4 14.8% 1 03.4%
Memory 9 07.0% 3 04.9% 3 11.1% 0 0%
Confusion 8 06.3% 5 08.2% 3 11.1% 2 06.9%
Prior transient ischemic 1 .8% 1 01.6% 0 0% 1 03.4%
attack (TIA)
Visual field
Finger perimetry 66 51.6% 29 47.5% 14 51.9% 11 37.9%
Oculomotoric
No conjugated bulbi 2 01.6% 1 01.6% 1 03.7% 0 0%
Diplopic images 8 06.3% 2 03.3% 1 03.7% 0 0%
Pursuit to left impaired 11 08.6% 3 04.9% 1 03.7% 2 06.9%
Pursuit to right impaired 15 11.7% 3 04.9% 1 03.7% 2 06.9%
Pursuit (up) impaired 6 04.7% 1 01.6% 0 0% 1 03.4%
Pursuit (down) impaired 4 03.1% 1 01.6% 0 0% 1 03.4%
Saccades to left imp. (t) 7 05.5% 2 03.3% 0 0% 2 06.9%
Saccades to left imp. (s) 13 10.2% 5 08.2% 2 07.4% 3 10.3%
Saccades to right imp. (t) 10 07.8% 3 04.9% 2 07.4% 1 03.4%
Saccades to right imp. (s) 17 13.3% 5 08.2% 3 11.1% 2 06.9%
Grasping
Left impaired 4 03.1% 3 04.9% 0 0% 3 10.3%
Right impaired 7 05.5% 3 04.9% 2 07.4% 1 03.4%
Extinction
Visual (left) 8 06.3% 4 06.6% 0 0% 4 13.8%
Visual (right) 6 04.7% 2 03.3% 2 07.4% 0 0%
Acoustic (left) 6 04.7% 2 03.3% 1 03.7% 1 03.4%
Acoustic (right) 2 01.6% 1 01.6% 1 03.7% 0 0%
Tactile (left) 2 01.6% 1 01.6% 0 0% 1 03.4%
Tactile (right) 1 .8% 1 01.6% 1 03.7% 0 0%
Neglect
Fixated view 2 01.6% 0 0% 0 0% 0 0%
Fixated head 2 01.6% 1 01.6% 0 0% 1 03.4%
No spont. movements 5 03.9% 2 03.3% 1 03.7% 1 03.4%
No eye contact 3 02.3% 0 0% 0 0% 0 0%

Results of neurological and neuro-ophthalmological examinations of all patients (column 1), of all patients with a delineated lesion (column 2)
and of all patients with left-hemispheric or right-hemispheric delineated lesions (column 3 and column 4, respectively).

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 7

Table 5 e Subjective impairments.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 128 61 27 29
Subjective Impairment
Memory 25 19.5% 12 19.7% 7 25.9% 3 10.3%
Anomia 33 25.8% 19 31.1% 13 48.1% 4 13.8%
Reading 58 45.3% 23 37.7% 13 48.1% 9 31.0%
Subjective visual impairment
Visual field defect 67 52.3% 25 41.0% 12 44.4% 11 37.9%
Spatial orientation 21 16.4% 10 16.4% 6 22.2% 3 10.3%
Eye-hand-coordination 17 13.3% 6 09.8% 2 07.4% 3 10.3%
Motion perception 9 07.0% 3 04.9% 2 07.4% 1 03.4%
Prosopagnosia 3 02.3% 2 03.3% 1 03.7% 1 03.4%
Color 6 04.7% 3 04.9% 0 0% 2 06.9%
Stereo 13 10.2% 5 08.2% 2 07.4% 2 06.9%
Phosphenes 43 33.6% 24 39.3% 12 44.4% 10 34.5%
Hallucinations 9 07.0% 3 04.9% 2 07.4% 1 03.4%

Subjective impairments of all patients (column 1), of all patients with a delineated lesion (column 2) and of all patients with left-hemispheric or
right-hemispheric delineated lesions (column 3 and column 4, respectively).

phosphenes were also correlated with a lesion of the primary For the Demtect, VLSM results of patients with a relevant
visual cortex BA 17 and lesion of the corpus callosum to deficit as compared to unimpaired patients are illustrated in
a minimal extent. Fig. 4. Voxels associated with a memory deficit are located in
Extended neurological, neuro-ophthalmological and neu- the hippocampus, parahippocampal gyrus and fusiform gyrus
ropsychological testing were carried out in 101 patients. (BA 18, 19, 20 and 37) and lesions of the cingulum, IFOF, ILF as
Findings are summarized in Table 6. Overall, nine scotomas well as the corpus callosum (to a minimal extent), respectively
and eight quadrantanopias were detected by automated (see Supplementary Fig. 4).
perimetry but missed by finger perimetry. The lesion topo- For the ROCF recall, a VLSM could not be performed,
graphy for patients who had no versus distinct visual field since only eight of the patients with delineated lesions
defects is illustrated in Fig. 3. showed a relevant deficit. A subtraction analysis revealed no
Half of all patients obtained normal results in the Lang specific area associated with a deficit in ROCF immediate
Stereo Test, while the remaining patients were either recall (see Supplementary Fig. 5). Note that half of our
completely impaired [failure to recognize any of the three patients with a deficit in ROCF showed no deficit in the
figures (cat ¼ 1200”, star ¼ 600”, car ¼ 600” disparity)], or Demtect.
partially impaired (failure to recognize at least one of the
figures). Subtraction analysis revealed no specific cortical area
associated with a partial or complete deficit in the Lang Stereo 4. Discussion
Test (see Supplementary Fig. 2).
In the clinical context occipital, occipito-temporal and
3.4. Neuropsychological symptoms occipito-parietal infarction is often perceived as being asso-
ciated with hemianopia alone. In a large patient collective
The majority of patients showed no deficits in the screening with such lesions we showed that patients often exhibited
tests, in the ROCF copy and in the FPT. Approximately a third additional clinical signs and symptoms: Apart from a visual
of our patients showed pathological results in the covert field defect and seeing phosphenes, patients reported
attention test (TAP) and in the Demtect, and a fifth showed subjective deficits such as anomia, reading disorders and
a deficit in the ROCF recall (see Table 7). memory deficits. Overall, the results of our study are
For the TAP, a relationship was found between lesion size congruent with previous studies which report neuro-
and slowed reaction times in the delineated lesion group. psychological and neurological deficits after occipital,
Lesion size was significantly greater for patients with general occipito-temporal and occipito-parietal infarction (Brandt
slowing compared to patients with generally intact processing et al., 2000; Cals et al., 2002; Kumral et al., 2004). Yet, this
speed (2864 voxels vs 1758 voxels, p < .05, t-test) and with study considerably extends our knowledge about occipital,
slowing after invalid cues (3265 voxels vs 1975 voxels occipito-temporal and occipito-parietal infarction through
p < .05, t-test). VLSM revealed no significant correlations. detailed descriptions of infarct topography, neurological,
Supplementary Fig. 3 displays the results of a lesion subtrac- neuropsychological symptoms, and importantly, the defini-
tion analysis for patients with generally slowed reaction times tion of anatomical correlates of neuropsychological dysfunc-
versus patients whose reactions became slowed only after tion by using a lesion-symptom mapping approach.
invalid cues in the covert attention test. Both general slowing Topographically, a visual field defect, a reading disorder,
and slowing after invalid cues were associated with lesions in and the perception of phosphenes (see also Baier et al.,
the lingual gyrus. 2010a) were associated with lesions of the calcarine sulcus.

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
8 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

Fig. 2 e Subjective impairments. Results of the statistical voxelwise lesion-behavior mapping analysis for subjective
memory deficits (first line), subjective anomia (second line), subjective reading disorder (third line), subjective visual field
defects (fourth line) and subjective perception of phosphenes (fifth line). Note that left-hemispheric lesions are flipped to the
right side. The Liebermeister test statistics were used as implemented in the MRICron software. Voxels that were damaged
significantly more often in patients showing the deficit than in patients with no deficit are color-coded in red after
adjustment for multiple comparisons. The range of z-values indicating significance (p < .05), as well as the corresponding
anatomical regions (BA) are given on the right hand side for each subjective impairment.

Anomia and memory deficits were associated with lesions of and U-shaped tracts can lead to alexia, lesions of the ILF or
the occipital inferior gyrus, or the lingual gyrus and hippo- IFOF can lead to surface dyslexia (Epelbaum et al., 2008;
campus (see also Szabo et al., 2009). Hodologically, a visual Coltheart et al., 1983; ffytche et al., 2010) and visual amnesia
field defect, a reading disorder and the perception of phos- occurs after lesions of the ILF or IFOF (Ross, 1980; ffytche
phenes were correlated with lesions of the corpus callosum. et al., 2010). As in the current study, memory deficits have
Memory deficits were associated with lesions of the IFOF, ILF been found to be predominantly associated with left-
and cingulum. These findings are in accordance with hemispheric lesions by Cals et al. (2002). Although reports
previous studies, suggesting that lesions of the ILF, splenium of hippocampal lesions after stroke are rare, a recent study of

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 9

Table 6 e Objective neurological and neuro-ophthalmological impairments.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 101 48 23 22
Neurological impairment
Visual field defect 54 53.5% 22 45.8% 12 52.2% 8 36.4%
(finger perimetry)
Visual acuity
Visus (near) binocular 1.00  .3 1.05  .26 1.09  .22 .99  .30
Visus (far) best out of 2 eyes .88  .3 .92  .25 .97  .28 .90  .24
Automatic static perimetry
Free visual field 31 30.7% 18 37.5% 7 30.4% 10 45.5%
Complete hemianopia 9 08.9% 1 02.1% 1 04.3% 0 0%
Incomplete hemianopia 18 17.8% 5 10.4% 4 17.4% 1 04.5%
Quadrantanopia 29 28.7% 15 31.3% 8 34.8% 5 22.7%
Scotoma 14 13.9% 9 18.8% 3 13.0% 6 27.3%
Color vision
Ishihara impaired 9 08.9% 2 04.2% 1 04.3% 1 04.5%
Stereo vision (Lang)
Intact 50 49.5% 22 45.8% 13 56.5% 8 36.4%
Partially intact 22 21.8% 11 22.9% 6 26.1% 5 22.7%
Impaired 21 20.8% 11 22.9% 3 13.0% 6 27.3%
Out (amblyopia/strabismus) 8 07.9% 4 08.3% 1 04.3% 3 13.6%
Cat impaired 42 41.6% 25 52.1% 10 43.5% 13 59.1%
Star impaired 32 31.7% 15 31.3% 5 21.7% 8 36.4%
Car impaired 36 35.6% 18 37.5% 5 21.7% 11 50.0%

Objective neurological and neuro-ophthalmological impairments of all patients (column 1), of all patients with a delineated lesion (column 2)
and of all patients with left-hemispheric or right-hemispheric delineated lesions (column 3 and column 4, respectively).

Szabo et al. (2009), which reported 57 cases of hippocampal 4.1. Conclusion and perspectives
infarction, demonstrated that careful neuropsychological
testing revealed memory deficits for both left- and right- This study underlines the importance of neuropsychological
hemispheric lesions of the hippocampus. In their study as deficits far beyond a visual field defect that are to be expected
well, lesions were not restricted to the hippocampus. after infarctions in this location. Screening tests for reading,
Instead, they also affected the occipital cortex or the memory deficits and visual deficits can be easily applied by
perpendicular thalamus. Importantly, verbal memory was any neurologist. We propose a combination of a reading test,
affected more frequently after left-hemispheric lesions, the Demtect, the ROCF Test and the Lang Stereo Test, as well
which is consistent with our results. as an anomia test (anamnesis) as the standard test battery
In the study by Szabo et al. (2009), spatial memory as following occipital infarction. Testing time would not exceed
measured by the ROCF was more frequently impaired in 20 min. If screening tests show positive results, a neuropsy-
patients with right-hemispherical-hippocampal-lesions. In chologist should be involved to investigate whether or not the
contrast, our results indicate that a deficit in ROCF immedi- severity of the patients’ impairment required rehabilitation
ate recall does not necessitate a right-hemispherical- measures, by administering a more complex neuro-
hippocampal-lesion. A number of studies also discussed that psychological test battery. For interpretation of the Demtect
the ROCF measures verbal memory, as the figural parts can be results, it is very important to check whether the hippo-
verbalized (e.g., McConley et al., 2008). Half of our patients campus is affected after occipital infarction. Moreover, since
with a deficit in ROCF showed no deficit in the Demtect. This visual field defects, especially scotoma and quadrantanopia
clearly shows that ROCF immediate recall and the Demtect may remain undetected using finger perimetry, we suggest
measure, to a certain extent, distinct deficits. that automated perimetry should be performed for all patients
Standard screening tests such as the line bisection, with occipital infarction (see also Townend et al., 2007).
cancellation and FPT are less sensitive for deficits in the In our view, lesion-symptom mapping in larger samples of
subacute period after occipital infarction. These tests might be patients or in specific subgroups will continue to expand our
more sensitive for identifying deficits in MCA patients, if understanding of clinico-anatomical relationships in the
larger parts of the parietal cortex are affected (but see also occipital lobes and beyond. While the current study reported
Baier et al., 2010b). the relation of a broad spectrum of neuropsychological deficits
We found that a general slowing in the TAP correlates with to lesions of cortical areas as well as white matter structures
lesion size, but not with a specific cortical area. This result is in a descriptive manner, further insights may be gained by
consistent with previous reports of attention research. For more detailed analyses of the exact contribution of cortical
example, Habekost and Rostrup (2007) showed that large versus white matter lesions for a particular deficit. For
strokes and extended leukoaraiosis can be related to bilateral example, regression analyses may help in discerning whether
deficits in the processing speed of visual attention. memory deficits after occipital infarction are more likely to

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
10 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

Fig. 3 e Topography of visual field defects as revealed by automated perimetry. Results of overlap analysis for patients with
no visual field defect (first line), hemianopia (second line), quadrantanopia (third line) and scotoma (fourth line). Note that
left-hemispheric lesions are flipped to the right side.

develop after lesions to the hippocampus itself or to nearby 4.2. Study limitations
tracts such as the ILF. Furthermore, 3D volumes of interest
will be needed for each lesion to be able to use this technique In the current study, the interval between infarction and time
in a statistically meaningful way. of testing varies between patients. The majority of patients
At present, it remains an open question whether or not were tested in the subacute phase at least 24 h after stroke.
specific visual disorders concerning color, motion or stereo Future follow-up studies should address which symptoms can
perception, as reported by patients, are indeed rare (see also be consistently observed in distinct time windows after
Cals et al., 2002; Kumral et al., 2004) or if they simply cannot be occipital infarction.
appropriately diagnosed with standard screening tests. Diag- VLSM was performed only for patients without severe
nosis, differentiation and lesion-symptom mapping of specific cortical atrophy, multiple cerebral or subcortical lesions or
visual deficits such as color, motion or stereo perception, as severe white matter lesions (N ¼ 61). Given these selection
well as higher visual cognitive disorders, may need more criteria the mean age of the VLSM group was 56.4 years, which
specialized testing (e.g., Kraft et al., 2010) by highly skilled is both below the mean age of the total group and below the
neuropsychologists or neurologists. common age for stroke in general.

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 11

Table 7 e Neuropsychological impairments.

All patients All delineated lesions Left-hemispheric lesions Right-hemispheric lesions

N 101 48 23 22
Screening tests
Cancellation impaired 5 05.0% 0 0% 0 0% 0 0%
Line bisection impaired 12 11.9% 2 04.2% 0 0% 1 04.5%
Clock drawing impaired 21 20.8% 3 06.3% 2 08.7% 1 04.5%
Clock drawing (neglect-like) 1 01.0% 0 0% 0 0% 0 0%
FPT
Intact 69 68.3% 38 79.2% 19 82.6% 17 77.3%
Impaired þ1 SD 17 16.8% 5 10.4% 1 04.3% 4 18.2%
Impaired þ2 SD 7 06.9% 2 04.2% 1 04.3% 0 0%
Missing 8 07.9% 3 06.3% 2 08.7% 1 04.5%
ROCF copy (mean percentile) 75.8  31.2 83.3  26.9 87.5  23.5 79.6  29.2
.1e100 .1e100 7.0e100 .1e100
PR < 2 2 02.0% 1 02.1% 0 0% 1 04.5%
PR < 16 4 04.0% 1 02.1% 1 04.3% 0 0%
PR < 84 34 33.7% 13 27.1% 4 17.4% 8 36.4%
PR < 98 24 23.8% 11 22.9% 8 34.8% 3 13.6%
PR > 98 36 35.6% 21 43.8% 10 43.5% 9 40.9%
Missing 1 01.0% 1 02.1% 0 0% 1 04.5%
Covert attention TAP
Slowed generally 36 35.6% 19 39.6% 11 47.8% 6 27.3%
Slowed invalid cues 27 26.7% 9 18.8% 3 13.0% 5 22.7%
Side difference 21 20.8% 5 10.4% 2 08.7% 2 09.1%
Missing 8 07.9% 5 10.4% 5 21.7% 1 04.5%
Demtect (age-matched norm values)
Intact 66 65.3% 37 77.1% 15 65.2% 20 90.9%
MCI 25 24.8% 8 16.7% 6 26.1% 1 04.5%
Dementia (suspicion) 9 08.9% 3 06.3% 2 08.7% 1 04.5%
Missing 1 01.0% 0 0% 0 0% 0 0%
Word imm. recall (max. 3) 2.53  .7 2.58  .7 2.39  .9 2.82  .4
Numbers (max. 3) 2.47  .7 2.58  .6 2.57  .7 2.64  .6
Supermarket (max. 4) 3.48  1.0 3.52  1.1 3.34  1.2 3.64  1.0
Digits backward (max. 3) 2.62  .6 2.65  .6 2.70  .6 2.59  .7
Word del. recall (max. 5) 2.34  1.9 2.67  1.8 2.17  1.9 3.27  1.6
ROCF immediate recall 35.1  35.8 38.6  35.3 34.8  34.5 39.9  37.3
(mean percentile) 0e99 0e99 .5e99 0e99
PR < 2 21 20.8% 8 16.7% 4 17.4% 4 18.2%
PR < 16 27 26.7% 11 22.9% 6 26.1% 5 22.7%
PR < 84 35 34.7% 19 39.6% 9 39.1% 8 36.4%
PR < 98 11 10.9% 6 12.5% 2 08.7% 3 13.6%
PR > 98 5 05.0% 2 04.2% 1 04.3% 1 04.5%
Missing 2 02.0% 2 04.2% 1 04.3% 1 04.5%

Neuropsychological impairments of all patients (column 1), of all patients with a delineated lesion (column 2) and of all patients with left-
hemispheric or right-hemispheric delineated lesions (column 3 and column 4, respectively).

Fig. 4 e Demtect. Results of the statistical voxelwise lesion-behavior mapping analysis for patients with mild cognitive
impairment (MCI) or dementia suspicion as compared to unimpaired patients. The Liebermeister test statistics were used.
Voxels that were damaged significantly more often in patients showing the deficit than in patients with no deficit are color-
coded red after adjustment for multiple comparisons. The range of z-values indicating significance (p < .05), as well as the
corresponding anatomical regions (BA) are given on the right hand side. Left-hemispheric lesions are flipped to the right
side.

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
12 c o r t e x x x x ( 2 0 1 2 ) 1 e1 3

Since patients were recruited in two different study Benson DF, Marsden CD, and Meadows JC. The amnesic
centers, imaging was performed at different scanners with syndrome of posterior cerebral artery occlusion. Acta
slightly different scanning parameters for the respective Neurologica Scandinavica, 50(2): 133e145, 1974.
Billino J, Braun DI, Bremmer F, and Gegenfurtner KR. Challenges
sequences. This difference in scanning parameters may have
to normal neural functioning provide insights into separability
lowered the precision for the VLSM analyses. Ideally, future of motion processing mechanisms. Neuropsychologia, 49(12):
studies should use the same scanning parameters at different 3151e3163, 2011.
study sites. Bird CM, Malhotra P, Parton A, Coulthard E, Rushworth MF, and
Because high resolution MRI scans were available only for Husain M. Visual neglect after right posterior cerebral artery
a minority of our patients, VLSM and analyses of white matter infarction. Journal of Neurology, Neurosurgery & Psychiatry, 77(9):
tract damage were performed on the basis of manually 1008e1012, 2006.
Brandt T, Steinke W, Thie A, Pessin MS, and Caplan LR. Posterior
delineated 2D multilayer ROI. To improve both precision and
cerebral artery territory infarcts: Clinical features, infarct
statistical power future studies should use unified high reso- topography, causes and outcome. Multicenter results and
lution MR images for all patients. a review of the literature. [Review]. Cerebrovascular Diseases,
Differences in lesion topography between left- and right- 10(3): 170e182, 2000.
hemispheric lesions may be explained by a selection bias. Bürgel U, Amunts K, Hoemke L, Mohlberg H, Gilsbach JM, and
First, while left-hemispheric temporomesial lesions Zilles K. White matter fiber tracts of the human brain: Three-
dimensional mapping at microscopic resolution, topography
(including both temporomesial projections as well as the
and intersubject variability. NeuroImage, 29(4): 1092e1105, 2006.
hippocampus itself) have been clearly associated with clini-
Cals N, Devuyst G, Afsar N, Karapanayiotides T, and
cally evident memory deficits (von Cramon et al., 1988), right- Bogousslavsky J. Pure superficial posterior cerebral artery
hemispheric lesions of the same location seem to remain territory infarction in the Lausanne Stroke Registry. Journal of
asymptomatic more often, leading to fewer presentation to Neurology, 249(7): 855e861, 2002.
hospital and, therefore, less frequent inclusion to our study. Carlesimo GA, Casadio P, Sabbadini M, and Caltagirone C.
Second, left-hemispheric occipito-parietal lesions usually Associative visual agnosia resulting from a disconnection
between intact visual memory and semantic systems. Cortex,
caused by infarction in the MCA territory often result in
34(4): 563e576, 1998.
aphasia, which was an important exclusion criterion of the Chechlacz M, Rotshtein P, Hansen PC, Deb S, Riddoch MJ, and
present study. Humphreys GW. The central role of the temporo-parietal
junction and the superior longitudinal fasciculus in
supporting multi-item competition: Evidence from lesion-
symptom mapping of extinction. Cortex, in press
Acknowledgments Coltheart M, Masterson J, Byng S, Prior M, and Riddoch J. Surface
dyslexia. The Quarterly Journal of Experimental Psychology A,
This work was supported by the German Research Foundation Human Experimental Psychology, 35: 469e495, 1983.
(BR 1691/5-1 and FA 119/17-1). We thank M. Sengutta, Epelbaum S, Pinel P, Gaillard R, Delmaire C, Perrin M, Dupont S, et al.
Pure alexia as a disconnection syndrome: New diffusion imaging
I. Käthner, M. Hanke and Y. Schaar for assistance in data
evidence for an old concept. Cortex, 44(8): 962e974, 2008.
acquisition. We wish to thank M. Catani and M. Thiebaut de ffytche DH, Blom JD, and Catani M. Disorders of visual perception.
Schotten for useful suggestions and advice on the white Journal of Neurology, Neurosurgery & Psychiatry, 81(11):
matter tract analysis. We thank two anonymous reviewers for 1280e1287, 2010.
useful criticisms on the original version of the manuscript. We Girkin CA and Miller NR. Central disorders of vision in humans.
thank J. England for corrections to the English text. Survey of Ophthalmology, 45(5): 379e405, 2001.
Gloning I, Gloning K, and Hoff H. Neuropsychological Symptoms and
Syndromes in Lesion of the Occipital Lobe and Adjacent Areas. Paris:
Gauthier-Villars, 1966.
Supplementary data Habekost T and Rostrup E. Visual attention capacity after right
hemisphere lesions. Neuropsychologia, 45(7): 1474e1488, 2007.
Supplementary data related to this article can be found at Habekost T and Starrfelt R. Alexia and quadrant-amblyopia:
http://dx.doi.org/10.1016/j.cortex.2012.10.004. Reading disability after a minor visual field deficit.
Neuropsychologia, 44(12): 2465e2476, 2006.
Holt LJ and Anderson SF. Bilateral occipital lobe stroke with
inferior altitudinal defects. Optometry, 71(11): 690e702, 2000.
references Ishihara S. Tests for Colour-blindness. Handaya, Tokyo: Hongo
Harukicho, 1917.
Kalbe E, Kessler J, Calabrese P, Smith R, Passmore AP, Brand M, et al.
Baier B, de Haan B, Mueller N, Thoemke F, Birklein F, Dieterich M, DemTect: A new, sensitive cognitive screening test to support
et al. Anatomical correlate of positive spontaneous visual the diagnosis of mild cognitive impairment and early dementia.
phenomena: A voxelwise lesion study. Neurology, 74(3): International Journal of Geriatric Psychiatry, 19(2): 136e143, 2004.
218e222, 2010a. Kalénine S, Buxbaum LJ, and Coslett HB. Critical brain regions for
Baier B, Mueller N, Fechir M, and Dieterich M. Line bisection action recognition: Lesion symptom mapping in left
error and its anatomic correlate. Stroke, 41(7): 1561e1563, hemisphere stroke. Brain, 133(11): 3269e3280, 2010.
2010b. Karnath HO, Himmelbach M, and Rorden C. The subcortical
Baldo JV, Arévalo A, Patterson JP, and Dronkers NF. Grey and anatomy of human spatial neglect: Putamen, caudate nucleus
white matter correlates of picture naming: Evidence from and pulvinar. Brain, 125(Pt 2): 350e360, 2002.
a voxel-based lesion analysis of the Boston Naming Test. Karnath HO, Fruhmann Berger M, Küker W, and Rorden C. The
Cortex, in press anatomy of spatial neglect based on voxelwise statistical

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004
c o r t e x x x x ( 2 0 1 2 ) 1 e1 3 13

analysis: A study of 140 patients. Cerebral Cortex, 14(10): Pflugshaupt T, Gutbrod K, Wurtz P, von Wartburg R, Nyffeler T, de
1164e1172, 2004. Haan B, et al. About the role of visual field defects in pure
Karnath HO, Rennig J, Johannsen L, and Rorden C. The anatomy alexia. Brain, 132(Pt 7): 1907e1917, 2009.
underlying acute versus chronic spatial neglect: A longitudinal Pillon B, Bakchine S, and Lhermitte F. Alexia without agraphia in
study. Brain, 134(Pt 3): 903e912, 2011. a left-handed patient with a right occipital lesion. Archives of
Kessler J, Schaaf A, and Mielke R. Fragmentierter Bildertest. Neurology, 44(12): 1257e1262, 1987.
Göttingen: Hogrefe, 1993. Ptak R, Di Pietro M, and Schnider A. The neural correlates of
Konen CS, Behrmann M, Nishimura M, and Kastner S. The object-centered processing in reading: a lesion study of
functional neuroanatomy of object agnosia: A case study. neglect dyslexia. Neuropsychologia, 50(6): 1142e1150, 2012.
Neuron, 71(1): 49e60, 2011. Rorden C, Karnath HO, and Bonilha L. Improving lesion-symptom
Kumral E, Bayulkem G, Ataç C, and Alper Y. Spectrum of mapping. Journal of Cognitive Neuroscience, 19(7): 1081e1088, 2007.
superficial posterior cerebral artery territory infarcts. European Ross ED. Sensory-specific and fractional disorders of recent
Journal of Neurology, 11(4): 237e246, 2004. memory in man I. Isolated loss of visual recent memory.
Kraft A, Grimsen C, Trenner D, Kehrer S, Lipfert A, Köhnlein M, Archives of Neurology, 37(4): 193e200, 1980.
et al. Specificity of fast perceptual learning in shape Rowe F, Brand D, Jackson CA, Price A, Walker L, Harrison S, et al.
localisation tasks based on detection versus form Visual impairment following stroke: Do stroke patients
discrimination. Vision Research, 50(4): 473e478, 2010. require vision assessment? Age and Ageing, 38: 188e193, 2009.
Landis T, Cummings JL, Benson DF, and Palmer EP. Loss of Shin MS, Park SY, Park SR, Seol SH, and Kwon JS. Clinical and
topographic familiarity. An environmental agnosia. Archives of empirical applications of the ReyeOsterrieth Complex
Neurology, 43(2): 132e136, 1986. Figure Test. Nature Protocols, 1(2): 892e899, 2006.
Lang J. Mikrostrabismus. Bücherei des Augenarztes, Heft 62. Stuttgart: Steinke W, Mangold J, Schwartz A, and Hennerici M. Mechanisms
Enke, 1982. of infarction in the superficial posterior cerebral artery
Machner B, Sprenger A, Kömpf D, Sander T, Heide W, Kimmig H, territory. Journal of Neurology, 244(9): 571e578, 1997.
et al. Visual search disorders beyond pure sensory failure in Szabo K, Förster A, Jäger T, Kern R, Griebe M, Hennerici MG, et al.
patients with acute homonymous visual field defects. Hippocampal lesion patterns in acute posterior cerebral artery
Neuropsychologia, 47(13): 2704e2711, 2009. stroke: Clinical and MRI findings. Stroke, 40(6): 2042e2045,
Maulaz AB, Bezerra DC, and Bogousslavsky J. Posterior cerebral 2009.
artery infarction from middle cerebral artery infarction. Thiebaut de Schotten M, ffytche DH, Bizzi A, Dell’Acqua F,
Archives of Neurology, 62: 938e941, 2005. Allin M, Walshe M, et al. Atlasing location, asymmetry and
McConley R, Martin R, Palmer CA, Kuzniecky R, Knowlton R, and inter-subject variability of white matter tracts in the human
Faught E. Rey Osterrieth complex figure test spatial and figural brain with MR diffusion tractography. NeuroImage, 54(1):
scoring: Relations to seizure focus and hippocampal pathology 49e59, 2011.
in patients with temporal lobe epilepsy. Epilepsy and Behavior, Tomaiuolo F, Voci L, Bresci M, Cozza S, Posteraro F, Oliva M, et al.
13(1): 174e177, 2008. Selective visual neglect in right brain damaged patients with
Milandre L, Brosset C, Botti G, and Khalil R. Etude de 82 infarctus splenial interhemispheric disconnection. Experimental Brain
du territoire des artéres cérébrales potérieures. Revue Research, 206(2): 209e217, 2010.
Neurologique (Paris), 150: 133e141, 1994. Tombini M, Pellegrino G, Zappasodi F, Quattrocchi CC,
Molenberghs P and Sale MV. Testing for spatial neglect with line Assenza G, Melgari JM, et al. Complex visual hallucinations
bisection and target cancellation: Are both tasks really after occipital extrastriate ischemic stroke. Cortex, 48(6):
unrelated? PLoS One, 6(7): e23017, 2011. 774e777, 2011.
Ntaios G, Spengos K, Vemmou AM, Savvari P, Koroboki E, Townend BS, Sturm JW, Petsoglou C, O’Leary B, Whyte S, and
Stranjalis G, et al. Long-term outcome in posterior cerebral Crimmins D. Perimetric homonymous visual field loss post-
artery stroke. European Journal of Neurology, 8(8): 1074e1080, 2011. stroke. Journal of Clinical Neuroscience, 14: 754e756, 2007.
Ohtake H, Fujii T, Yamadori A, Fujimori M, Hayakawa Y, and von Cramon DY, Hebel N, and Schuri U. Verbal memory and
Suzuki K. The influence of misnaming on object recognition: A learning in unilateral posterior cerebral infarction. A report on
case of multimodal agnosia. Cortex, 37(2): 175e186, 2001. 30 cases. Brain, 111(Pt 5): 1061e1077, 1988.
Park KC, Lee BH, Kim EJ, Shin MH, Choi KM, Yoon SS, et al. Wahlund LO, Barkhof F, Fazekas F, Bronge L, Augustin M,
Deafferentationedisconnection neglect induced by posterior Sjögren M, et al. A new rating scale for age-related white
cerebral artery infarction. Neurology, 66(1): 56e61, 2006. matter changes applicable to MRI and CT. Stroke, 32(6):
Park KC, Yoon SS, and Seo KH. Splenium or parahippocampus 1318e1322, 2001.
involvement and its relationship to cognitive decline in Yamamoto Y, Georgiadis AL, Chang HM, and Caplan LR. Posterior
posterior cerebral artery infarction. Journal of Clinical cerebral artery territory infarcts in the New England Medical
Neuroscience, 16(7): 914e917, 2009. Center Posterior Circulation Registry. Archives of Neurology,
Park KC, Yoon SS, and Rhee HY. Executive dysfunction associated 56(7): 824e832, 1999.
with stroke in the posterior cerebral artery territory. Journal of Zihl J and von Cramon D. Zerebrale Sehstörungen. Stuttgart:
Clinical Neuroscience, 18: 203e208, 2011. Kohlhammer, 1986.
Pessin MS, Lathi ES, Cohen MB, Kwan ES, Hedges 3rd TR, and Zimmermann P and Fimm B. Testbatterie zur
Caplan LR. Clinical features and mechanism of occipital Aufmerksamkeitsprüfung (TAP). Version 1.02. Handbuch Teil 1.
infarction. Annals of Neurology, 21(3): 290e299, 1987. Freiburg: Psytest, 1993.

Please cite this article in press as: Kraft A, et al., Neurological and neuropsychological characteristics of occipital, occipito-
temporal and occipito-parietal infarction, Cortex (2012), http://dx.doi.org/10.1016/j.cortex.2012.10.004

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