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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.cortexjournal.net/?rss=yes"><title>Cortex</title><description>Cortex RSS feed: Current Issue. 
 CORTEX  is an international journal devoted to the study of cognition and
of the relationship between the nervous system and mental 
processes,
particularly as these are reflected in the behaviour of patients with
acquired brain lesions, normal volunteers, children 
with typical and
atypical development, and in the activation of brain regions and systems
as recorded by functional neuroimaging techniques.

It was founded in 1964 by Ennio De Renzi.</description><link>http://www.cortexjournal.net/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Cortex</prism:publicationName><prism:issn>0010-9452</prism:issn><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:publicationDate>September 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945210001619/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945210001620/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945210001644/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209000379/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS001094520900224X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002159/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002494/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002172/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002445/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002536/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945210000808/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945209002834/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS001094521000081X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cortexjournal.net/article/PIIS0010945210000547/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945210001619/abstract?rss=yes"><title>Cover Figure</title><link>http://www.cortexjournal.net/article/PIIS0010945210001619/abstract?rss=yes</link><description></description><dc:title>Cover Figure</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0010-9452(10)00161-9</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e1</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945210001620/abstract?rss=yes"><title>Editorial Board/Title Page</title><link>http://www.cortexjournal.net/article/PIIS0010945210001620/abstract?rss=yes</link><description></description><dc:title>Editorial Board/Title Page</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0010-9452(10)00162-0</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945210001644/abstract?rss=yes"><title>Contents</title><link>http://www.cortexjournal.net/article/PIIS0010945210001644/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0010-9452(10)00164-4</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iii</prism:startingPage><prism:endingPage>iv</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209000379/abstract?rss=yes"><title>Does history repeat itself? Cortical columns: 4. Déja vu?</title><link>http://www.cortexjournal.net/article/PIIS0010945209000379/abstract?rss=yes</link><description>‘Those who fail to learn the lessons of history are doomed to repeat them’George Santayana   We ended part 3 of this sequence of editorials by Smith (Cortex 46/6) by quoting  opinion (subsequently somewhat softened) that the cerebral cortex was as a ‘quasi-crystalline structure’. Each cortical column (macrocolumn) was said to have a diameter of about 300μm and to contain some 7500–8000 neurons (subdivided into about 80 minicolumns, which were said to form the recurring unit). This organisation, and magnitude, remains remarkably constant from mouse to man. In the visual cortex Hubel and Wiesel suggested that the organisation resembled nothing so much as an ‘ice-tray’ where each complete 180° set of orientation columns constituted an ‘orientation hypercolumn’ and, similarly, the two ocular dominance columns constituted an ‘ocular dominance hypercolumn’. The two hypercolumns together can, they proposed, ‘be considered an elementary unit of the primary visual cortex’. This idea was popularised some ten years later in David  very successful book, Eye Brain and Vision, 1988: p. 131. As in all popularisations, the caveats in the original tend to be lost. In their  were careful to point out that ‘orientation columns may vary continuously…and we have no evidence that they intersect at right angles’.</description><dc:title>Does history repeat itself? Cortical columns: 4. Déja vu?</dc:title><dc:creator>Christopher U.M. Smith</dc:creator><dc:identifier>10.1016/j.cortex.2009.02.002</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-03-04</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-03-04</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>947</prism:startingPage><prism:endingPage>948</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS001094520900224X/abstract?rss=yes"><title>Three cases of developmental prosopagnosia from one family: Detailed neuropsychological and psychophysical investigation of face processing</title><link>http://www.cortexjournal.net/article/PIIS001094520900224X/abstract?rss=yes</link><description>Abstract: A number of reports have documented that developmental prosopagnosia (DP) can run in families, but the locus of the deficits in those cases remains unclear. We investigated the perceptual basis of three cases of DP from one family (67 year-old father FA, and two daughters, 39 year-old D1 and 34 year-old D2) by combining neuropsychological and psychophysical methods. Neuropsychological tests involving natural facial images demonstrated significant face recognition deficits in the three family members. All three members showed normal facial expression recognition and face detection, and two of them (D2, FA) performed well on within-class object recognition tasks. These individuals were then examined in a series of psychophysical experiments. Intermediate form vision preceding face perception was assessed with radial frequency (RF) patterns. Normal discrimination of RF patterns in these individuals indicates that their face recognition difficulties are higher in the cortical form vision hierarchy than the locus of contour shape processing. Psychophysical experiments requiring discrimination and memory for synthetic faces aimed to quantify their face processing abilities and systematically examine the representation of facial geometry across viewpoints. D1 showed deficits in perceiving geometric information from the face at a given view. D2's impairments seem to arise in later face processing stages involving transferring view-dependent descriptions into a view-invariant representation. FA performed poorly on face learning and recognition relative to the age-appropriate controls. These cases provide evidence for familial transmission of high-level visual recognition deficits with normal intermediate-level form vision.</description><dc:title>Three cases of developmental prosopagnosia from one family: Detailed neuropsychological and psychophysical investigation of face processing</dc:title><dc:creator>Yunjo Lee, Bradley Duchaine, Hugh R. Wilson, Ken Nakayama</dc:creator><dc:identifier>10.1016/j.cortex.2009.07.012</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-09-03</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-09-03</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>949</prism:startingPage><prism:endingPage>964</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002159/abstract?rss=yes"><title>Acquired prosopagnosia abolishes the face inversion effect</title><link>http://www.cortexjournal.net/article/PIIS0010945209002159/abstract?rss=yes</link><description>Abstract: Individual faces are notoriously difficult to recognize when they are presented upside-down. Since acquired prosopagnosia (AP) has been associated with an impairment of expert face processes, a reduced or abolished face inversion effect (FIE) is expected in AP. However, previous studies have incongruently reported apparent normal effects of inversion, a decreased or abolished FIE, but also a surprisingly better performance for inverted faces for some patients. While these discrepant observations may be due to the variability of high-level processes impaired, a careful look at the literature rather suggests that the pattern of FIE in prosopagnosia has been obscured by a selection of patients with associated low-level defects and general visual recognition impairments, as well as trade-offs between accuracy and correct RT measures. Here we conducted an extensive investigation of upright and inverted face processing in a well-characterized case of face-selective AP, PS (). In 4 individual face discrimination experiments, PS did not present any inversion effect at all, taking into account all dependent measures of performance. However, she showed a small inversion cost for individualizing members of a category of non-face objects (cars), just like normal observers. A fifth experiment with personally familiar faces to recognize confirmed the lack of inversion effect for PS. Following the present report and a survey of the literature, we conclude that the FIE is generally absent, or at least clearly reduced following AP. We also suggest that the paradoxical superior performance for inverted faces observed in rare cases may be due to additional upper visual field defects rather than to high-level competing visual processes. These observations are entirely compatible with the view that AP is associated with a disruption of a process that is also abolished following inversion: the holistic representation of individual exemplars of the face class.</description><dc:title>Acquired prosopagnosia abolishes the face inversion effect</dc:title><dc:creator>Thomas Busigny, Bruno Rossion</dc:creator><dc:identifier>10.1016/j.cortex.2009.07.004</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-08-17</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-08-17</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>965</prism:startingPage><prism:endingPage>981</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002494/abstract?rss=yes"><title>Is the visual analyzer orthographic-specific? Reading words and numbers in letter position dyslexia</title><link>http://www.cortexjournal.net/article/PIIS0010945209002494/abstract?rss=yes</link><description>Abstract: Letter position dyslexia (LPD) is a deficit in the encoding of letter position within words. It is characterized by errors of letter migration within words, such as reading trail as trial and form as from. In order to examine whether LPD is domain-specific, and to assess the domain-specificity of the visual analysis system, this study explored whether LPD extends to number reading, by testing whether individuals who have letter migrations in word reading also show migrations while reading numbers. The reading of words and numbers of 12 Hebrew-speaking individuals with developmental LPD was assessed. Experiment 1 tested reading aloud of words and numbers, and Experiment 2 tested same–different decisions in words and numbers. The findings indicated that whereas the participants with developmental LPD showed a large number of migration errors in reading words, 10 of them read numbers well, without migration errors, and not differently from the control participants. A closer inspection of the pattern of errors in words and numbers of two individuals who had migrations in both numbers and words showed qualitative differences in the characteristics of migration errors in the two types of stimuli. In word reading, migration errors appeared predominantly in middle letters, whereas the errors in numbers occurred mainly in final (rightmost) digits. Migrations in numbers occurred almost exclusively in adjacent digits, but in words migrations occurred both in adjacent and in nonadjacent letters. The results thus indicate that words can be selectively impaired, without a parallel impairment in numbers, and that even when numbers are also impaired they show different error pattern. Thus, the visual analyzer is actually an orthographic visual analyzer, a module that is domain-specific for the analysis of words.</description><dc:title>Is the visual analyzer orthographic-specific? Reading words and numbers in letter position dyslexia</dc:title><dc:creator>Naama Friedmann, Dror Dotan, Einav Rahamim</dc:creator><dc:identifier>10.1016/j.cortex.2009.08.007</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-10-26</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-10-26</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>982</prism:startingPage><prism:endingPage>1004</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002172/abstract?rss=yes"><title>Functional neuroanatomy of the encoding and retrieval processes of verbal episodic memory in MCI</title><link>http://www.cortexjournal.net/article/PIIS0010945209002172/abstract?rss=yes</link><description>Abstract: Introduction: The goal of this study was to explore the association between disease severity and performance on brain activation associated with episodic memory encoding and retrieval in persons with mild cognitive impairment (MCI).Method: This was achieved by scanning 12 MCI persons and 10 age- and education-matched healthy controls while encoding words and while retrieving them in a recognition test.Results: Behaviorally, there was no significant group difference on recognition performance. However, MCI and healthy controls showed different patterns of cerebral activation during encoding. While most of these differences demonstrated reduced activation in the MCI group, there were areas of increased activation in the left ventrolateral prefrontal cortex. Reduced activation was found in brain areas known to be either structurally compromised or hypometabolic in Alzheimer's disease (AD). In contrast, very few group differences were associated with retrieval. Correlation analyses indicated that increased disease severity, as measured with the Mattis Dementia Rating Scale, was associated with smaller activation of the right middle and superior temporal gyri. In contrast, recognition success in MCI persons was associated with larger activation of the left ventrolateral prefrontal cortex during the encoding phase.Conclusion: Overall, our results indicate that most of the memory-related cerebral network changes in MCI persons occur during the encoding phase. They also suggest that a prefrontal compensatory mechanism could occur in parallel with the disease-associated reduction of cerebral activation in temporal areas.</description><dc:title>Functional neuroanatomy of the encoding and retrieval processes of verbal episodic memory in MCI</dc:title><dc:creator>Francis Clément, Sylvie Belleville, Samira Mellah</dc:creator><dc:identifier>10.1016/j.cortex.2009.07.003</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-08-17</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-08-17</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>1005</prism:startingPage><prism:endingPage>1015</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002445/abstract?rss=yes"><title>Different motor imagery modes following brain damage</title><link>http://www.cortexjournal.net/article/PIIS0010945209002445/abstract?rss=yes</link><description>Abstract: In recent years, many researches have explored the relationship between overt and covert motor activity (i.e., mental simulation). Consistent evidence has been provided in favour of close similarities between the two functions, particularly based on behavioural and neuroimaging studies on healthy participants. Interestingly, literature on the pathological population remains largely controversial. Yet, a clear understanding of whether and how mental simulation is modified by overt motor disorders is far from a speculative question, especially in view of the increasing interest for the use of mental practice in motor rehabilitation. Here, we explored whether a single set of cognitive skills is applied while solving tasks that implicitly require mental simulation of an action, or whether alternative strategies might be elicited according to the imager's actual motor capabilities. For this purpose, we recruited a group of patients who suffered from a stroke affecting selectively either the right or the left hemisphere, responsible for motor impairments ranging in severity. We required them, and a group of age-matched healthy controls, to perform a task of simulated grasping, and two tasks involving handedness judgments (on hands and gloves, respectively). Dissociations were found between the performances of patients suffering from left versus right brain damage, according to the task and, interestingly, the actual state of the imager's motor capabilities. This finding suggests that motor imagery might include alternative mental strategies that are independent from the actual state of the motor system. We discuss how these mental operations are differently affected by motor impairment, and consider the implications of the present theoretical finding for neurorehabilitation.</description><dc:title>Different motor imagery modes following brain damage</dc:title><dc:creator>Elena Daprati, Daniele Nico, Sylvie Duval, Francesco Lacquaniti</dc:creator><dc:identifier>10.1016/j.cortex.2009.08.002</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-09-03</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-09-03</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>1016</prism:startingPage><prism:endingPage>1030</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002536/abstract?rss=yes"><title>The closing-in phenomenon in the drawing performance of Alzheimer's disease patients: A compensation account</title><link>http://www.cortexjournal.net/article/PIIS0010945209002536/abstract?rss=yes</link><description>Abstract: Introduction: The closing-in phenomenon, first described by  as a tendency to close in on models while performing a constructional task, occurs with a relatively high frequency in patients with dementia. The phenomenon may appear in several tasks, but it is more usually observed in tests of copying drawings. In the present study we examined the hypothesis that in patients with Alzheimer's disease (AD) the phenomenon may be related to particularly severe visuo-spatial dysfunction.Methods: Thirty-nine of an overall sample of 382 patients consecutively admitted to an AD unit exhibited closing-in in their copying drawings performance. The presence of closing-in was diagnosed when, in at least one of three drawings, the copy touched, in one or more parts, the model.Results: With respect to another group of 39 AD patients with constructional apraxia but who showed no closing-in behaviour, patients with closing-in showed more severe impairment on several tests of visuo-spatial abilities. The two groups did not differ in the frequency of neurological primitive reflexes or performance on tests of executive functioning.Conclusions: The present study supports the interpretation that the closing-in phenomenon in patients with AD is a compensatory strategy to overcome basic visuo-spatial dysfunctions involved in the preliminary visuo-perceptual analysis and/or in the on-line maintenance of the visual representation of the model while performing a copying drawing task. Possible limits in the conclusions of the present study are related to the retrospective nature of the present study and to the choice of considering only overlap-type forms of closing behaviour.</description><dc:title>The closing-in phenomenon in the drawing performance of Alzheimer's disease patients: A compensation account</dc:title><dc:creator>Laura Serra, Lucia Fadda, Roberta Perri, Carlo Caltagirone, Giovanni A. Carlesimo</dc:creator><dc:identifier>10.1016/j.cortex.2009.08.010</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2009-09-28</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2009-09-28</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Research Reports</prism:section><prism:startingPage>1031</prism:startingPage><prism:endingPage>1036</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945210000808/abstract?rss=yes"><title>Epileptic feeling of multiple presences in the frontal space</title><link>http://www.cortexjournal.net/article/PIIS0010945210000808/abstract?rss=yes</link><description>Abstract: We describe the case of a patient who during a simple focal epileptic seizure due to vascular cerebral sequelae, reported the paroxysmal convincing feeling of the presence of several familiar persons in her peripersonal and extrapersonal space. Because the patient reported sensing multiple presences and recognizing them as family members, her case appears to contradict the hypothesis that the feeling of a non-existent human presence is an autoscopic phenomenon involving the neural “reduplication of the body”. As an alternative hypothesis, I propose that the feeling of a non-existent presence may be only a hallucination of an ordinary “perception of the presence of another”. Otherwise, the closest presence was felt in front of the patient, without lateralization in one hemispace, suggesting the importance to take into account other spatial dimensions than the left/right dimension, such as the front/back dimension, in the feeling of a presence. Illusory perceptive phenomena could participate in future in better understanding brain regions involved in the front/back dimension of the space perceptive representation.</description><dc:title>Epileptic feeling of multiple presences in the frontal space</dc:title><dc:creator>Fabienne Picard</dc:creator><dc:identifier>10.1016/j.cortex.2010.02.002</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-03-22</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-03-22</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Note</prism:section><prism:startingPage>1037</prism:startingPage><prism:endingPage>1042</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945209002834/abstract?rss=yes"><title>Margaret Kennard (1899–1975): Not a ‘Principle’ of brain plasticity but a founding mother of developmental neuropsychology</title><link>http://www.cortexjournal.net/article/PIIS0010945209002834/abstract?rss=yes</link><description>Abstract: According to the ‘Kennard Principle’, there is a negative linear relation between age at brain injury and functional outcome. Other things being equal, the younger the lesioned organism, the better the outcome. But the ‘Kennard Principle’ is neither Kennard's nor a principle. In her work, Kennard sought to explain the factors that predicted functional outcome (age, to be sure, but also staging, laterality, location, and number of brain lesions, and outcome domain) and the neural mechanisms that altered the lesioned brain's functionality. This paper discusses Kennard's life and years at Yale (1931–1943); considers the genesis and scope of her work on early-onset brain lesions, which represents an empirical and theoretical foundation for current developmental neuropsychology; offers an historical explanation of why the ‘Kennard Principle’ emerged in the context of early 1970s work on brain plasticity; shows why uncritical belief in the ‘Kennard Principle’ continues to shape current research and practice; and reviews the continuing importance of her work.</description><dc:title>Margaret Kennard (1899–1975): Not a ‘Principle’ of brain plasticity but a founding mother of developmental neuropsychology</dc:title><dc:creator>Maureen Dennis</dc:creator><dc:identifier>10.1016/j.cortex.2009.10.008</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-01-18</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-01-18</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Historical Paper</prism:section><prism:startingPage>1043</prism:startingPage><prism:endingPage>1059</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS001094521000081X/abstract?rss=yes"><title>Are special issue papers more cited?</title><link>http://www.cortexjournal.net/article/PIIS001094521000081X/abstract?rss=yes</link><description>Citation bias is a hot topic. According to ScienceDirect (http://www.sciencedirect.com) an astonishing 10,000 plus articles have been published with the term ‘citation bias’ in the all-field search (between 1980 and 2010). Citation count is often used as marker of the scientific quality of a given paper and is also used to judge its impact on the scientific community. So much so, in fact, that the number of papers published and the number of associated citations may even influence the allocation of research funding and spending – on a worldwide basis (). Importantly, the number of times a paper is cited directly influences a journal's impact factor. Impact factor is determined by dividing the total number of citations in a given year by the total number of source items in the preceding two years or five years (). But citation bias may flaw the entire system.</description><dc:title>Are special issue papers more cited?</dc:title><dc:creator>Joanna Brooks, Sergio Della Sala</dc:creator><dc:identifier>10.1016/j.cortex.2010.02.003</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-03-15</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-03-15</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Discussion Forum</prism:section><prism:startingPage>1060</prism:startingPage><prism:endingPage>1064</prism:endingPage></item><item rdf:about="http://www.cortexjournal.net/article/PIIS0010945210000547/abstract?rss=yes"><title>Scriptwriter's amnesia: Autobiographical memory loss in the documentary film Unknown White Male (2005)</title><link>http://www.cortexjournal.net/article/PIIS0010945210000547/abstract?rss=yes</link><description>Writers of fictional stories know about both the dramatic and comic effects that can be generated by creating amnesic syndromes for characters. Viewers of cinema and television become well-acquainted with the phenomenon of scriptwriter's amnesia, and do not need special medical or psychological knowledge to understand that it is quite different from the usual types of memory loss that are caused by brain disease. In a recent article titled ‘Memories aren't made of this: amnesia at the movies’,  highlighted common elements of these representations of amnesia:</description><dc:title>Scriptwriter's amnesia: Autobiographical memory loss in the documentary film Unknown White Male (2005)</dc:title><dc:creator>Peter A. Kempster, Helene L. Roberts</dc:creator><dc:identifier>10.1016/j.cortex.2010.01.010</dc:identifier><dc:source>Cortex 46, 8 (2010)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Cortex</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate><prism:volume>46</prism:volume><prism:number>8</prism:number><prism:issueIdentifier>S0010-9452(10)X0007-7</prism:issueIdentifier><prism:section>Book and New Media Review</prism:section><prism:startingPage>1065</prism:startingPage><prism:endingPage>1068</prism:endingPage></item></rdf:RDF>