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            "title": "Connected speech as a marker of disease progression in autopsy-proven Alzheimer’s disease",
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                    "creatorType": "author",
                    "firstName": "Samrah",
                    "lastName": "Ahmed"
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                    "creatorType": "author",
                    "firstName": "Anne-Marie F.",
                    "lastName": "Haigh"
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                    "firstName": "Celeste A. de",
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            "abstractNote": "Although an insidious history of episodic memory difficulty is a typical presenting symptom of Alzheimer’s disease, detailed neuropsychological profiling frequently demonstrates deficits in other cognitive domains, including language. Previous studies from our group have shown that language changes may be reflected in connected speech production in the earliest stages of typical Alzheimer’s disease. The aim of the present study was to identify features of connected speech that could be used to examine longitudinal profiles of impairment in Alzheimer’s disease. Samples of connected speech were obtained from 15 former participants in a longitudinal cohort study of ageing and dementia, in whom Alzheimer’s disease was diagnosed during life and confirmed at post-mortem. All patients met clinical and neuropsychological criteria for mild cognitive impairment between 6 and 18 months before converting to a status of probable Alzheimer’s disease. In a subset of these patients neuropsychological data were available, both at the point of conversion to Alzheimer’s disease, and after disease severity had progressed from the mild to moderate stage. Connected speech samples from these patients were examined at later disease stages. Spoken language samples were obtained using the Cookie Theft picture description task. Samples were analysed using measures of syntactic complexity, lexical content, speech production, fluency and semantic content. Individual case analysis revealed that subtle changes in language were evident during the prodromal stages of Alzheimer’s disease, with two-thirds of patients with mild cognitive impairment showing significant but heterogeneous changes in connected speech. However, impairments at the mild cognitive impairment stage did not necessarily entail deficits at mild or moderate stages of disease, suggesting non-language influences on some aspects of performance. Subsequent examination of these measures revealed significant linear trends over the three stages of disease in syntactic complexity, semantic and lexical content. The findings suggest, first, that there is a progressive disruption in language integrity, detectable from the prodromal stage in a subset of patients with Alzheimer’s disease, and secondly that measures of semantic and lexical content and syntactic complexity best capture the global progression of linguistic impairment through the successive clinical stages of disease. The identification of disease-specific language impairment in prodromal Alzheimer’s disease could enhance clinicians’ ability to distinguish probable Alzheimer’s disease from changes attributable to ageing, while longitudinal assessment could provide a simple approach to disease monitoring in therapeutic trials.",
            "publicationTitle": "Brain",
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            "date": "12/01/2013",
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            "pages": "3727-3737",
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            "title": "Cognitive control and its impact on recovery from aphasic stroke",
            "creators": [
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                    "creatorType": "author",
                    "firstName": "Sonia L. E.",
                    "lastName": "Brownsett"
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                    "creatorType": "author",
                    "firstName": "Jane E.",
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                    "firstName": "Zoe",
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                    "creatorType": "author",
                    "firstName": "Robert",
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                },
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                    "creatorType": "author",
                    "firstName": "Richard J. S.",
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            "abstractNote": "Aphasic deficits are usually only interpreted in terms of domain-specific language processes. However, effective human communication and tests that probe this complex cognitive skill are also dependent on domain-general processes. In the clinical context, it is a pragmatic observation that impaired attention and executive functions interfere with the rehabilitation of aphasia. One system that is important in cognitive control is the salience network, which includes dorsal anterior cingulate cortex and adjacent cortex in the superior frontal gyrus (midline frontal cortex). This functional imaging study assessed domain-general activity in the midline frontal cortex, which was remote from the infarct, in relation to performance on a standard test of spoken language in 16 chronic aphasic patients both before and after a rehabilitation programme. During scanning, participants heard simple sentences, with each listening trial followed immediately by a trial in which they repeated back the previous sentence. Listening to sentences in the context of a listen–repeat task was expected to activate regions involved in both language-specific processes (speech perception and comprehension, verbal working memory and pre-articulatory rehearsal) and a number of task-specific processes (including attention to utterances and attempts to overcome pre-response conflict and decision uncertainty during impaired speech perception). To visualize the same system in healthy participants, sentences were presented to them as three-channel noise-vocoded speech, thereby impairing speech perception and assessing whether this evokes domain general cognitive systems. As expected, contrasting the more difficult task of perceiving and preparing to repeat noise-vocoded speech with the same task on clear speech demonstrated increased activity in the midline frontal cortex in the healthy participants. The same region was activated in the aphasic patients as they listened to standard (undistorted) sentences. Using a region of interest defined from the data on the healthy participants, data from the midline frontal cortex was obtained from the patients. Across the group and across different scanning sessions, activity correlated significantly with the patients’ communicative abilities. This correlation was not influenced by the sizes of the lesion or the patients’ chronological ages. This is the first study that has directly correlated activity in a domain general system, specifically the salience network, with residual language performance in post-stroke aphasia. It provides direct evidence in support of the clinical intuition that domain-general cognitive control is an essential factor contributing to the potential for recovery from aphasic stroke.",
            "publicationTitle": "Brain",
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            "title": "Changes in sexual functioning from 6 to 12 months following traumatic brain injury: a prospective TBI model system multicenter study",
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                    "firstName": "Robin A",
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                    "firstName": "Kacey L",
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            "abstractNote": "OBJECTIVE: To investigate longitudinal changes in sexual functioning during the first year following moderate to severe traumatic brain injury (TBI).\nDESIGN: Prospective cohort study.\nSETTING: Community.\nPARTICIPANTS: 182 persons (53 women and 129 men) with moderate to severe TBI who were admitted to 1 of 6 participating TBI Model System centers and followed in the community at 6 and 12 months after injury.\nMAIN MEASURES: Derogatis Interview for Sexual Functioning-Self-Report (DISF-SR); Global Sexual Satisfaction Index (GSSI).\nRESULTS: Mean T-scores on the DISF-SR Arousal subscale demonstrated marginal improvement over time, with a 2.59-point increase (P = .05) from 6 to 12 months after injury. There were no significant differences over this 6-month period on the remaining DISF-SR subscales, including sexual cognition/fantasy, sexual behavior/experience, and orgasm. There was no significant change in satisfaction with sexual functioning on the GSSI from 6 months (72% satisfied) to 12 months (71% satisfied).\nCONCLUSIONS AND IMPLICATIONS: Sexual function and satisfaction appears to be stable in those with moderate to severe TBI from 6 to 12 months after injury, with the exception of minimal improvement in arousal. These findings, to our knowledge, reflect the first evidence regarding prospective changes in sexual functioning in this population. Future research can go far to assist clinicians in treatment planning and managing patient expectations of recovery of sexual functioning after TBI.",
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                }
            ],
            "abstractNote": "Complex movement (CM) refers to the representation of a goal-oriented action and is classified as either transitive (use of tools) or intransitive (communication gestures). Both types of CM have three specific components: temporal, spatial, and content, which are subdivided into specific error types (SET). Since there is debate regarding the contribution of each brain hemisphere for the types of CM, our objective was to describe the brain lateralization of components and SET of transitive and intransitive CM. We studied 14 patients with a left hemisphere stroke (LH), 12 patients with a right hemisphere stroke (RH), and 16 control subjects. The Florida Apraxia Screening Test-Revised (FAST-R, Rothi et al., 1988) was used for the assessment of CM. Both clinical groups showed a worse performance than the control group on the total FAST-R and transitive movement scores (p<0.001). Failures in Spatial and Temporal components were found in both clinical groups, but only LH patients showed significantly more Content errors (p<0.01) than the control group. Also, only the LH group showed a higher number of errors for intransitive movements score (p=0.017), due to lower scores in the content component, compared to the control group (p=0.04). Transitive and intransitive CMs differ in their neurocognitive representation; transitive CM shows a bilateral distribution of its components when compared to intransitive CM, which shows a preferential left hemisphere representation. This could result from higher neurocognitive demands for movements that require use of tools, compared with more automatic communication gestures.",
            "publicationTitle": "Brain and cognition",
            "publisher": "",
            "place": "",
            "date": "Dec 30, 2013",
            "volume": "84",
            "issue": "1",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "164-169",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Brain Cogn",
            "DOI": "10.1016/j.bandc.2013.11.010",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "1090-2147",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "Brain lateralization of complex movement",
            "language": "ENG",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
            "extra": "PMID: 24384089",
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            "creatorSummary": "Rafaels et al.",
            "parsedDate": "2012-10",
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            "version": 55,
            "itemType": "journalArticle",
            "title": "Brain injury risk from primary blast",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Karin A",
                    "lastName": "Rafaels"
                },
                {
                    "creatorType": "author",
                    "firstName": "Cameron R Dale",
                    "lastName": "Bass"
                },
                {
                    "creatorType": "author",
                    "firstName": "Matthew B",
                    "lastName": "Panzer"
                },
                {
                    "creatorType": "author",
                    "firstName": "Robert S",
                    "lastName": "Salzar"
                },
                {
                    "creatorType": "author",
                    "firstName": "William A",
                    "lastName": "Woods"
                },
                {
                    "creatorType": "author",
                    "firstName": "Sanford H",
                    "lastName": "Feldman"
                },
                {
                    "creatorType": "author",
                    "firstName": "Tim",
                    "lastName": "Walilko"
                },
                {
                    "creatorType": "author",
                    "firstName": "Richard W",
                    "lastName": "Kent"
                },
                {
                    "creatorType": "author",
                    "firstName": "Bruce P",
                    "lastName": "Capehart"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jonathan B",
                    "lastName": "Foster"
                },
                {
                    "creatorType": "author",
                    "firstName": "Burcu",
                    "lastName": "Derkunt"
                },
                {
                    "creatorType": "author",
                    "firstName": "Amanda",
                    "lastName": "Toman"
                }
            ],
            "abstractNote": "BACKGROUND: Military service members are often exposed to at least one explosive event, and many blast-exposed veterans present with symptoms of traumatic brain injury. However, there is little information on the intensity and duration of blast necessary to cause brain injury.\nMETHODS: Varying intensity shock tube blasts were focused on the head of anesthetized ferrets, whose thorax and abdomen were protected. Injury evaluations included physiologic consequences, gross necropsy, and histologic diagnosis. The resulting apnea, meningeal bleeding, and fatality were analyzed using logistic regressions to determine injury risk functions.\nRESULTS: Increasing severity of blast exposure demonstrated increasing apnea immediately after the blast. Gross necropsy revealed hemorrhages, frequently near the brain stem, at the highest blast intensities. Apnea, bleeding, and fatality risk functions from blast exposure to the head were determined for peak overpressure and positive-phase duration. The 50% risk of apnea and moderate hemorrhage were similar, whereas the 50% risk of mild hemorrhage was independent of duration and required lower overpressures (144 kPa). Another fatality risk function was determined with existing data for scaled positive-phase durations from 1 millisecond to 20 milliseconds.\nCONCLUSION: The first primary blast brain injury risk assessments for mild and moderate/severe injuries in a gyrencephalic animal model were determined. The blast level needed to cause a mild/moderate brain injury may be similar to or less than that needed for pulmonary injury. The risk functions can be used in future research for blast brain injury by providing realistic injury risks to guide the design of protection or evaluate injury.",
            "publicationTitle": "The journal of trauma and acute care surgery",
            "publisher": "",
            "place": "",
            "date": "Oct 2012",
            "volume": "73",
            "issue": "4",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "895-901",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "J Trauma Acute Care Surg",
            "DOI": "10.1097/TA.0b013e31825a760e",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "2163-0763",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
            "extra": "PMID: 22836001",
            "tags": [
                {
                    "tag": "Animals",
                    "type": 1
                },
                {
                    "tag": "Blast Injuries",
                    "type": 1
                },
                {
                    "tag": "Brain Injuries",
                    "type": 1
                },
                {
                    "tag": "Disease Models, Animal",
                    "type": 1
                },
                {
                    "tag": "Explosions",
                    "type": 1
                },
                {
                    "tag": "Ferrets",
                    "type": 1
                },
                {
                    "tag": "Male",
                    "type": 1
                },
                {
                    "tag": "Trauma Severity Indices",
                    "type": 1
                },
                {
                    "tag": "brain",
                    "type": 1
                }
            ],
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            "dateAdded": "2014-02-02T01:43:59Z",
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            "creatorSummary": "Wood et al.",
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        "data": {
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            "version": 54,
            "itemType": "journalArticle",
            "title": "Anxiety sensitivity and alexithymia as mediators of postconcussion syndrome following mild traumatic brain injury",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Rodger Ll",
                    "lastName": "Wood"
                },
                {
                    "creatorType": "author",
                    "firstName": "Geraldine",
                    "lastName": "Oʼhagan"
                },
                {
                    "creatorType": "author",
                    "firstName": "Claire",
                    "lastName": "Williams"
                },
                {
                    "creatorType": "author",
                    "firstName": "Michael",
                    "lastName": "McCabe"
                },
                {
                    "creatorType": "author",
                    "firstName": "Nicole",
                    "lastName": "Chadwick"
                }
            ],
            "abstractNote": "OBJECTIVE: To examine the influence of anxiety sensitivity (AS) and alexithymia as potential mediators for the development of psychological distress and postconcussion syndrome after mild traumatic brain injury (mTBI).\nPARTICIPANTS: Sixty-one patients with mTBI assessed at a mean of 2.38 weeks after injury and demographically matched healthy controls (n = 61).\nMEASURES: Twenty-item Toronto Alexithymia Scale, Anxiety Sensitivity Index, State-Trait Anxiety Inventory, and Rivermead Post Concussion Questionnaire.\nRESULTS: The mTBI group reported significantly higher levels of AS, alexithymia, psychological distress, and postconcussion (PC) symptom scores than controls. High AS and alexithymia in the mTBI group were associated with a greater number of PC symptoms and higher levels of psychological distress than patients scoring low on these measures and controls. In the mTBI group, a combination of AS and low mood explained 52.6% of the variance in PC symptom reporting. A combination of trait-anxiety, alexithymia, and PC symptoms explained 77.2% of the variance in levels of mood.\nCONCLUSION: A combination of low mood and high AS may act as a psychological diathesis for the development of persisting PC symptoms. Early identification could provide a focus for early intervention to prevent the development of postconcussion syndrome after mTBI.",
            "publicationTitle": "The Journal of head trauma rehabilitation",
            "publisher": "",
            "place": "",
            "date": "2014 Jan-Feb",
            "volume": "29",
            "issue": "1",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "E9-E17",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "J Head Trauma Rehabil",
            "DOI": "10.1097/HTR.0b013e31827eabba",
            "citationKey": "",
            "url": "",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
            "ISSN": "1550-509X",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "eng",
            "libraryCatalog": "NCBI PubMed",
            "callNumber": "",
            "rights": "",
            "extra": "PMID: 23381020",
            "tags": [],
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            "dateAdded": "2014-02-02T01:39:18Z",
            "dateModified": "2014-02-02T01:39:18Z"
        }
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    {
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            "creatorSummary": "Sanchez-Carrion et al.",
            "parsedDate": "2008-11-15",
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        "data": {
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            "version": 53,
            "itemType": "journalArticle",
            "title": "A longitudinal fMRI study of working memory in severe TBI patients with diffuse axonal injury",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Rocio",
                    "lastName": "Sanchez-Carrion"
                },
                {
                    "creatorType": "author",
                    "firstName": "Davinia",
                    "lastName": "Fernandez-Espejo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Carme",
                    "lastName": "Junque"
                },
                {
                    "creatorType": "author",
                    "firstName": "Carles",
                    "lastName": "Falcon"
                },
                {
                    "creatorType": "author",
                    "firstName": "Nuria",
                    "lastName": "Bargallo"
                },
                {
                    "creatorType": "author",
                    "firstName": "Teresa",
                    "lastName": "Roig"
                },
                {
                    "creatorType": "author",
                    "firstName": "Montserrat",
                    "lastName": "Bernabeu"
                },
                {
                    "creatorType": "author",
                    "firstName": "José M.",
                    "lastName": "Tormos"
                },
                {
                    "creatorType": "author",
                    "firstName": "Pere",
                    "lastName": "Vendrell"
                }
            ],
            "abstractNote": "Traumatic brain injury (TBI) patients have working memory deficits and altered patterns of brain activation during this function. The evolution of the impairment has not been examined to date. This study investigated longitudinal changes in brain activation during a working memory task. Twelve patients with severe and diffuse TBI and ten healthy matched controls were fMRI scanned twice at a 6-month interval during an n-back task (0-, 2- and 3-back). All the TBI patients selected presented signs of diffuse axonal injury on CT but had no evidence of focal lesions on MRI clinical examination. Significant changes in brain activation over time were observed in patients, but not in controls. During the first examination, though both groups engaged bilateral fronto-parietal regions known to be involved in working memory, activation of the right superior frontal gyrus was low in the TBI group. However, the difference between TBI and controls had decreased significantly after 6 months. A factor analysis confirmed the greater increase in activation in the right superior frontal cortex in the TBI group than in healthy controls, leading to normalization of the brain activation pattern. In conclusion, this longitudinal study provides evidence of a progressive normalization of the working memory activation pattern after diffuse axonal injury in severe TBI, coinciding with an improvement in performance on this function.",
            "publicationTitle": "NeuroImage",
            "publisher": "",
            "place": "",
            "date": "November 15, 2008",
            "volume": "43",
            "issue": "3",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "421-429",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "NeuroImage",
            "DOI": "10.1016/j.neuroimage.2008.08.003",
            "citationKey": "",
            "url": "http://www.sciencedirect.com/science/article/pii/S1053811908009063",
            "accessDate": "2013-12-23T17:19:52Z",
            "PMID": "",
            "PMCID": "",
            "ISSN": "1053-8119",
            "archive": "",
            "archiveLocation": "",
            "shortTitle": "",
            "language": "",
            "libraryCatalog": "ScienceDirect",
            "callNumber": "",
            "rights": "",
            "extra": "",
            "tags": [
                {
                    "tag": "Ddiffuse axonal injury",
                    "type": 1
                },
                {
                    "tag": "Working memory",
                    "type": 1
                },
                {
                    "tag": "functional MRI",
                    "type": 1
                },
                {
                    "tag": "longitudinal",
                    "type": 1
                },
                {
                    "tag": "traumatic brain injury",
                    "type": 1
                }
            ],
            "collections": [],
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            "dateAdded": "2014-02-02T00:58:31Z",
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            "creatorSummary": "Suntrup et al.",
            "parsedDate": "2013-03-01",
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        "data": {
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            "version": 52,
            "itemType": "journalArticle",
            "title": "Evidence for adaptive cortical changes in swallowing in Parkinson’s disease",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Sonja",
                    "lastName": "Suntrup"
                },
                {
                    "creatorType": "author",
                    "firstName": "Inga",
                    "lastName": "Teismann"
                },
                {
                    "creatorType": "author",
                    "firstName": "Joke",
                    "lastName": "Bejer"
                },
                {
                    "creatorType": "author",
                    "firstName": "Inga",
                    "lastName": "Suttrup"
                },
                {
                    "creatorType": "author",
                    "firstName": "Martin",
                    "lastName": "Winkels"
                },
                {
                    "creatorType": "author",
                    "firstName": "David",
                    "lastName": "Mehler"
                },
                {
                    "creatorType": "author",
                    "firstName": "Christo",
                    "lastName": "Pantev"
                },
                {
                    "creatorType": "author",
                    "firstName": "Rainer",
                    "lastName": "Dziewas"
                },
                {
                    "creatorType": "author",
                    "firstName": "Tobias",
                    "lastName": "Warnecke"
                }
            ],
            "abstractNote": "Dysphagia is a relevant symptom in Parkinson’s disease, whose pathophysiology is poorly understood. It is mainly attributed to degeneration of brainstem nuclei. However, alterations in the cortical contribution to deglutition control in the course of Parkinson’s disease have not been investigated. Here, we sought to determine the patterns of cortical swallowing processing in patients with Parkinson’s disease with and without dysphagia. Swallowing function in patients was objectively assessed with fiberoptic endoscopic evaluation. Swallow-related cortical activation was measured using whole-head magnetoencephalography in 10 dysphagic and 10 non-dysphagic patients with Parkinson’s disease and a healthy control group during self-paced swallowing. Data were analysed applying synthetic aperture magnetometry, and group analyses were done using a permutation test. Compared with healthy subjects, a strong decrease of cortical swallowing activation was found in all patients. It was most prominent in participants with manifest dysphagia. Non-dysphagic patients with Parkinson’s disease showed a pronounced shift of peak activation towards lateral parts of the premotor, motor and inferolateral parietal cortex with reduced activation of the supplementary motor area. This pattern was not found in dysphagic patients with Parkinson’s disease. We conclude that in Parkinson’s disease, not only brainstem and basal ganglia circuits, but also cortical areas modulate swallowing function in a clinically relevant way. Our results point towards adaptive cerebral changes in swallowing to compensate for deficient motor pathways. Recruitment of better preserved parallel motor loops driven by sensory afferent input seems to maintain swallowing function until progressing neurodegeneration exceeds beyond the means of this adaptive strategy, resulting in manifestation of dysphagia.",
            "publicationTitle": "Brain",
            "publisher": "",
            "place": "",
            "date": "03/01/2013",
            "volume": "136",
            "issue": "3",
            "section": "",
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            "abstractNote": "Parkinson’s disease is a chronic progressive neurodegenerative disorder characterized by resting tremor, slowness of movements, rigidity, gait disturbance and postural instability. Most investigations on Parkinson’s disease focused on the basal ganglia, whereas the cerebellum has often been overlooked. However, increasing evidence suggests that the cerebellum may have certain roles in the pathophysiology of Parkinson’s disease. Anatomical studies identified reciprocal connections between the basal ganglia and cerebellum. There are Parkinson’s disease–related pathological changes in the cerebellum. Functional or morphological modulations in the cerebellum were detected related to akinesia/rigidity, tremor, gait disturbance, dyskinesia and some non-motor symptoms. It is likely that the major roles of the cerebellum in Parkinson’s disease include pathological and compensatory effects. Pathological changes in the cerebellum might be induced by dopaminergic degeneration, abnormal drives from the basal ganglia and dopaminergic treatment, and may account for some clinical symptoms in Parkinson’s disease. The compensatory effect may help maintain better motor and non-motor functions. The cerebellum is also a potential target for some parkinsonian symptoms. Our knowledge about the roles of the cerebellum in Parkinson’s disease remains limited, and further attention to the cerebellum is warranted.",
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            "abstractNote": "Sensory neurons that respond to pleasant stimulation of the skin are not as well characterized as those that respond to noxious stimulation. Using calcium imaging in live mice, the authors of this study show that neurons in the skin that express the G protein-coupled receptor MRGPRB4 respond to pleasant stroking but not to pinching or poking stimuli.",
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            "creatorSummary": "Hachioui et al.",
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            "title": "Long-term prognosis of aphasia after stroke",
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                    "creatorType": "author",
                    "firstName": "Hanane El",
                    "lastName": "Hachioui"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hester F.",
                    "lastName": "Lingsma"
                },
                {
                    "creatorType": "author",
                    "firstName": "Mieke W. M. E. van de",
                    "lastName": "Sandt-Koenderman"
                },
                {
                    "creatorType": "author",
                    "firstName": "Diederik W. J.",
                    "lastName": "Dippel"
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                {
                    "creatorType": "author",
                    "firstName": "Peter J.",
                    "lastName": "Koudstaal"
                },
                {
                    "creatorType": "author",
                    "firstName": "Evy G.",
                    "lastName": "Visch-Brink"
                }
            ],
            "abstractNote": "Background The long-term functional outcome of aphasia after stroke is uncertain, even though this information is needed as early as possible for adequate patient care and support. This observational prospective study was aimed at predicting functional outcome at 1 year after stroke.\nMethods We examined linguistic components (ScreeLing) and functional verbal communication (Aphasia Severity Rating Scale, ASRS) in 147 aphasic patients. The ScreeLing was administered at 1, 2 and 6 weeks after stroke; the ASRS at 1 week and 1 year. The relationships between linguistic, demographic and stroke characteristics, and good functional outcome at 1 year (ASRS 4 or 5) were examined with logistic regression analyses.\nResults The baseline linguistic components (ie, semantics, phonology and syntax) were significant predictors (p<0.001) for 1-year outcome in univariable analyses. In multivariable analysis, these variables explained 46.5% of the variance, with phonology being the only significant predictor (p=0.003). Age, Barthel Index score, educational level and haemorrhagic stroke were identified as other significant predictors of outcome. A prognostic model of these five baseline predictors explained 55.7% of the variance. The internally validated area under the receiver operating characteristic curve (AUC) was 0.89, indicating good predictive performance. Adding the degree of phonological recovery between 1 and 6 weeks after stroke to this model increased the explained variance to 65% and the AUC to 0.91.\nConclusions The outcome of aphasia at 1 year after stroke can be predicted in the first week by the phonology score, the Barthel Index score, age, educational level and stroke subtype, with phonology being the strongest predictor.",
            "publicationTitle": "Journal of Neurology, Neurosurgery & Psychiatry",
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            "date": "03/01/2013",
            "volume": "84",
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            "journalAbbreviation": "J Neurol Neurosurg Psychiatry",
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            "creatorSummary": "Kauranen et al.",
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            "version": 49,
            "itemType": "journalArticle",
            "title": "The severity of cognitive deficits predicts return to work after a first-ever ischaemic stroke",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Tatu",
                    "lastName": "Kauranen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Katri",
                    "lastName": "Turunen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Siiri",
                    "lastName": "Laari"
                },
                {
                    "creatorType": "author",
                    "firstName": "Satu",
                    "lastName": "Mustanoja"
                },
                {
                    "creatorType": "author",
                    "firstName": "Peter",
                    "lastName": "Baumann"
                },
                {
                    "creatorType": "author",
                    "firstName": "Erja",
                    "lastName": "Poutiainen"
                }
            ],
            "abstractNote": "Background The inability of stroke patients to return to work contributes disproportionately to the socioeconomic impact of stroke and is best predicted by the severity of stroke. However, the role of cognitive deficits in stroke severity has not been scrutinised. We studied whether the initial cognitive severity of stroke, compared with other influential factors, predicts the inability to return to work after stroke.\nMethods Consecutive patients aged 18–65 with a first-ever ischaemic stroke, working full time previously, were assessed neuropsychologically within the first weeks after stroke and at the 6-month follow-up. Similarly, 50 healthy demographic controls were assessed twice. The cognitive severity of stroke was operationalised as the number of initial cognitive deficits. Cognitive severity as a predictor of the inability to return to work was compared with demographic, occupational, neurological, radiological and functional data, vascular risk factors and mood state.\nResults The mean age of the 140 patients assessed both initially and at follow-up was 52 years. They had a mean of 13 years of education and 59% were men. At 6 months, only 41% of the patients had returned to work despite the relatively minor neurological and functional impairments of the cohort. In our model, the number of early cognitive deficits (OR=2.252, CI 1.294 to 3.918) was the only significant predictor of the inability to return to work.\nConclusions The initial cognitive severity of stroke predicts the later inability to return to work. The benefits of neuropsychological assessments within the first weeks after stroke are emphasised.",
            "publicationTitle": "Journal of Neurology, Neurosurgery & Psychiatry",
            "publisher": "",
            "place": "",
            "date": "03/01/2013",
            "volume": "84",
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            "partTitle": "",
            "pages": "316-321",
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            "journalAbbreviation": "J Neurol Neurosurg Psychiatry",
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                    "tag": "Stroke",
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                {
                    "tag": "cerebrovascular disease",
                    "type": 1
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                    "tag": "cognition",
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            "version": 48,
            "itemType": "journalArticle",
            "title": "Depression and systemic lupus erythematosus: a systematic review",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "L",
                    "lastName": "Palagini"
                },
                {
                    "creatorType": "author",
                    "firstName": "M",
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                    "creatorType": "author",
                    "firstName": "C",
                    "lastName": "Tani"
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                    "creatorType": "author",
                    "firstName": "A",
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                    "firstName": "M",
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                    "firstName": "S",
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            ],
            "abstractNote": "ObjectiveSystemic lupus erythematosus (SLE) is a chronic, relapsing-remitting autoimmune disorder that involves multiple organ systems including the central nervous system. Among the items included in the nomenclature for neuropsychiatric SLE, mood disorders have been identified. The aim of this paper is to review the clinical and psychobiological relationship between depression and SLE.MethodWe performed a systematic search of MEDLINE, EMBASE, PsychINFO, using MeSH headings and keywords for 'depression' and 'SLE'.ResultsSeventeen studies reported depressive disorders, with prevalence rates in the range 17-75%. Three studies reported the most frequent symptoms, which may be represented by fatigue, weakness, somatic disorders and sleep disorders. Suicide ideation was much higher than in the general population. Nine studies analysed the relationship to SLE disease activity. The results of the available literature are contradictory. Psychobiological hypotheses have been considered in 13 studies. Among the psychobiological hypotheses which might underline the plausibility of their relationship, 'psychosocial factors' were the most frequently reported.ConclusionsDifferences in assessment techniques appear to be the main explanation for the variability in findings and important methodological limitations are present in the available literature to definitively point to the prevalence of depression, type of depression and most prevalent symptoms. To date, the relationship between depression and SLE disease activity also appears controversial. Methodological limitations are present in the available literature and it would be necessary to develop evidence-based guidelines to improve the diagnosis of depression in SLE. Identification of SLE-specific biomarkers of depression also has high priority.",
            "publicationTitle": "Lupus",
            "publisher": "",
            "place": "",
            "date": "Feb 20, 2013",
            "volume": "",
            "issue": "",
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            "seriesTitle": "",
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            "DOI": "10.1177/0961203313477227",
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            "shortTitle": "Depression and systemic lupus erythematosus",
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            "extra": "PMID: 23427220",
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            "dateAdded": "2013-06-07T21:53:28Z",
            "dateModified": "2013-06-07T21:53:28Z"
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            "title": "Demographic and motor features associated with the occurrence of neuropsychiatric and sleep complications of Parkinson's disease",
            "creators": [
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                    "creatorType": "author",
                    "firstName": "Renato Puppi",
                    "lastName": "Munhoz"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hélio A",
                    "lastName": "Teive"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hariklia",
                    "lastName": "Eleftherohorinou"
                },
                {
                    "creatorType": "author",
                    "firstName": "Lachlan J",
                    "lastName": "Coin"
                },
                {
                    "creatorType": "author",
                    "firstName": "Andrew J",
                    "lastName": "Lees"
                },
                {
                    "creatorType": "author",
                    "firstName": "Laura",
                    "lastName": "Silveira-Moriyama"
                }
            ],
            "abstractNote": "OBJECTIVE: To determine whether four key neuropsychiatric and sleep related features associated with Parkinson's disease (PD) are associated with the motor handicap and demographic data. BACKGROUND: The growing number of recognised non-motor features of PD makes routine screening of all these symptoms impractical. Here, we investigated the hypothesis that standard demographic data and the routine assessment of motor signs is associated with the presence of dementia, psychosis, clinically probable rapid eye movement (REM) sleep behavior disorder (cpRBD) and restless legs syndrome (RLS). METHODS: 775 patients with PD underwent standardised assessment of motor features and the presence of dementia, psychosis, cpRBD and RLS. A stepwise feature elimination procedure with fitted logistic regression models was applied to identify which/if any combination of demographic and motor factors is associated with each of the four studied non-motor features. A within-study out-of-sample estimate of the power of the predicted values of the models was calculated using standard evaluation procedures. RESULTS: Age and Hoehn&Yahr (H&Y) stage were strongly associated with the presence of dementia (p value<0.001 for both factors in the final selected model) while a combination of age, disease duration, H&Y stage, dopamine agonists and catechol-O-methyltransferase (COMT) inhibitors was associated with the presence of psychosis. Disease duration and H&Y stage were the significant indicators of cpRBD, and the lack of significant motor asymmetry was the only significant feature associated with RLS-type symptoms but the evidence of association was weak. CONCLUSIONS: Demographic and motor features routinely collected in patients with PD can estimate the occurrence of neuropsychiatric and sleep-related features of PD.",
            "publicationTitle": "Journal of neurology, neurosurgery, and psychiatry",
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