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<title>Journal of Neurology, Neurosurgery &#x26; Psychiatry current issue</title>
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<title>Journal of Neurology, Neurosurgery &#x26; Psychiatry</title>
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<title><![CDATA[Harlequin syndrome: does a cranial autonomic neuropathy influence headache?]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/577?rss=1</link>
<description><![CDATA[ <p>The paper by Viana <I>et al</I><cross-ref type="bib" refid="b1">1</cross-ref> analyses the relationship between Harlequin syndrome<cross-ref type="bib" refid="b2">2</cross-ref> and headache. One facet of this interesting syndrome is the demonstration of pupillary signs by pharmacological studies explicable by the sudden onset of parasympathetic and sympathetic deficit, implicating an autonomic neuropathy mediated by an autoimmune process or viral infection.<cross-ref type="bib" refid="b3">3</cross-ref></p> <p>Sympathetic innervation of human cerebral and extracranial circulation is well documented. Parasympathetic innervation of cranial arteries has been established in rat, cat and monkey, but information on humans is meagre. Stimulation of the pre- or post-ganglionic fibres of the sphenopalatine ganglion in animals increases cerebral blood flow, probably via orbital rami from the ganglion looping back to the internal carotid artery, and projecting directly to the external carotid artery.<cross-ref type="bib" refid="b4">4</cross-ref> A clinical marker of parasympathetic activity in man is the redness and lacrimation of the ipsilateral eye and discharge from the...]]></description>
<dc:creator><![CDATA[Drummond, P., Lance, J. W.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2012-302678</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2012-302678</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Immunology (including allergy), Headache (including migraine), Pain (neurology), Ophthalmology]]></dc:subject>
<dc:title><![CDATA[Harlequin syndrome: does a cranial autonomic neuropathy influence headache?]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Editorial commentaries</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>577</prism:startingPage>
<prism:endingPage>577</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/578?rss=1">
<title><![CDATA[Predicting MS progression: patience is a virtue]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/578?rss=1</link>
<description><![CDATA[ <p>Prediction of the rate of progression for an individual with multiple sclerosis (MS) is a difficult task due to the significant intrapersonal and interpersonal variability in the rate of change of disability. The most commonly used measure of disability is the expanded disability status score (EDSS),<cross-ref type="bib" refid="b1">1</cross-ref> which has been modified to take into account disease duration to produce the global multiple sclerosis severity score (MSSS), which has provided clinicians and researchers with a tool to quantify the degree of neurological disability for a given duration of MS.<cross-ref type="bib" refid="b2">2</cross-ref> However, the MSSS has not been validated as a longitudinal measure. The authors concluded that the MSSS could be used to measure and compare disease severity in groups of MS patients but that it had not yet been shown to be suitable for tracking an individual's progress over time. Therefore, there has been a significant need for a...]]></description>
<dc:creator><![CDATA[Taylor, B. V.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2012-302207</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2012-302207</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Immunology (including allergy), Multiple sclerosis]]></dc:subject>
<dc:title><![CDATA[Predicting MS progression: patience is a virtue]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Editorial commentaries</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>578</prism:startingPage>
<prism:endingPage>578</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/579?rss=1">
<title><![CDATA[A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project, 1981-86]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/579?rss=1</link>
<description><![CDATA[ <p><textbox><p><b>Title</b>: A PROSPECTIVE STUDY OF ACUTE CEREBROVASCULAR DISEASE IN THE COMMUNITY: THE OXFORDSHIRE COMMUNITY STROKE PROJECT, 1981&ndash;86<cross-ref type="bib" refid="b1">1</cross-ref></p> <p><b>Authors</b>: Bamford J, Sandercock P, Dennis M, Burn J, Warlow C</p> <p><b>Published</b>: 1988</p> </textbox></p> <p>Counting strokes in Oxfordshire: epidemiological rigour and neurological obsessiveness by Charles Warlow</p> <p>Citations are a slippery metric. Slippery to measure because citations from government papers, and books, are seldom counted. Slippery to interpret too. Are many citations because the paper was scientifically groundbreaking like the letter to <I>Nature</I> describing the structure of DNA? Or because it described a trial which changed the way large numbers of people should be treated&mdash;for example, by coiling rather than clipping to secure ruptured intracranial aneurysms? Or because the paper described a score which we all now use, like the Glasgow Coma Score, or a technique which changed the face of clinical neurology, like CT brain scanning? Or is it because...]]></description>
<dc:creator><![CDATA[Warlow, C. P.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301381</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301381</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Editor's choice, JNNP Impact commentaries, Coma and raised intracranial pressure, Infection (neurology), Stroke, Ischaemic heart disease, Radiology, Radiology (diagnostics)]]></dc:subject>
<dc:title><![CDATA[A prospective study of acute cerebrovascular disease in the community: the Oxfordshire Community Stroke Project, 1981-86]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Impact commentaries</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>579</prism:startingPage>
<prism:endingPage>579</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/580?rss=1">
<title><![CDATA[Brief screening tests during acute admission in patients with mild stroke are predictive of vascular cognitive impairment 3-6 months after stroke]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/580?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To determine the prognostic value of brief cognitive screening tests administered in the subacute stroke phase (initial 2&nbsp;weeks) for the detection of significant cognitive impairment 3&ndash;6&nbsp;months after stroke, the authors compared the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE).</p>
</sec>
<sec><st>Methods</st>
<p>Patients with ischaemic stroke and transient ischaemic attack were assessed with both MoCA and MMSE within 14&nbsp;days after index stroke, followed by a formal neuropsychological evaluation of seven cognitive domains 3&ndash;6&nbsp;months later. Cognitive outcomes were dichotomised as either no&ndash;mild (impairment in &le;2 cognitive domains) or moderate&ndash;severe (impairment in &ge;3 cognitive domains) vascular cognitive impairment. Area under the receiver operating characteristic (ROC) curve analysis was used to compare discriminatory ability.</p>
</sec>
<sec><st>Results</st>
<p>300 patients were recruited, of whom 239 received formal neuropsychological assessment 3&ndash;6&nbsp;months after the stroke. 60 (25%) patients had moderate&ndash;severe VCI. The overall discriminant validity for detection of moderate&ndash;severe cognitive impairment was similar for MoCA (ROC 0.85 (95% CI 0.79 to 0.90) and MMSE (ROC 0.83 (95% CI 0.77 to 0.89)), p=0.96). Both MoCA (21/22) and MMSE (25/26) had similar discriminant indices at their optimal cutoff points; sensitivity 0.88 versus 0.88; specificity 0.64 versus 0.67; 70% versus 72% correctly classified. Moreover, both tests had similar discriminant indices in detecting impaired cognitive domains.</p>
</sec>
<sec><st>Conclusions</st>
<p>Brief screening tests during acute admission in patients with mild stroke are predictive of significant vascular cognitive impairment 3&ndash;6&nbsp;months after stroke.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Dong, Y., Venketasubramanian, N., Chan, B. P.-L., Sharma, V. K., Slavin, M. J., Collinson, S. L., Sachdev, P., Chan, Y. H., Chen, C. L.-H.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-302070</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-302070</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Stroke, Memory disorders (psychiatry)]]></dc:subject>
<dc:title><![CDATA[Brief screening tests during acute admission in patients with mild stroke are predictive of vascular cognitive impairment 3-6 months after stroke]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Cerebrovascular disease</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>580</prism:startingPage>
<prism:endingPage>585</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/586?rss=1">
<title><![CDATA[Anterior choroidal artery ischaemic patterns predict outcome of carotid occlusion]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/586?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To investigate whether anterior choroidal artery (AChA) territory sparing or AChA infarction restricted to the medial temporal lobe (MT), implying good collateral status, predicts good outcome, defined as modified Rankin Scale 0&ndash;2, at discharge in acute internal carotid artery (ICA) occlusion.</p>
</sec>
<sec><st>Methods</st>
<p>The authors studied consecutive patients with acute ICA occlusion admitted to an academic medical centre between January 2002 and August 2010, who underwent MRI followed by conventional angiography. The pattern of AChA involvement on initial diffusion-weighted imaging was dichotomised as spared or MT only versus other partial or full. The association of AChA infarct patterns and good outcome at discharge was calculated by multivariate logistic regression with adjustment.</p>
</sec>
<sec><st>Results</st>
<p>For the 60 patients meeting entry criteria, mean age was 68.3&nbsp;years and median admission NIH Stroke Scale score was 19. AChA territory was spared or restricted to the MT in 27 patients and other partially involved or fully involved in 33 patients. AChA territory spared or ischaemia restricted to MT only, compared with other partial infarct patterns or full infarct, was independently associated with good discharge outcome (44.4% vs 12.1%, OR 7.24, 95% CI 1.32 to 39.89, p=0.023).</p>
</sec>
<sec><st>Conclusion</st>
<p>In acute ICA occlusion, the absence of AChA infarction or restriction to the MT is an independent predictor of good discharge outcome. Analysis of AChA infarct patterns may improve early prognostication and decision-making.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Lee, M., Saver, J. L., Hao, Q., Starkman, S., Salamon, N., Ali, L. K., Kim, D., Ovbiagele, B., Song, S., Raychev, R., Abcede, H., Fiaz, R., Liebeskind, D. S., for the UCLA Stroke Investigators]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301493</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301493</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Stroke, Ophthalmology, Radiology, Radiology (diagnostics)]]></dc:subject>
<dc:title><![CDATA[Anterior choroidal artery ischaemic patterns predict outcome of carotid occlusion]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Cerebrovascular disease</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>586</prism:startingPage>
<prism:endingPage>590</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/591?rss=1">
<title><![CDATA[Executive dysfunction in adults with moyamoya disease is associated with increased diffusion in frontal white matter]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/591?rss=1</link>
<description><![CDATA[
<sec><st>Background and purpose</st>
<p>Alteration of the cerebrovascular reserve (CVR) in the frontal lobes has been associated with cognitive dysfunction in adults with moyamoya disease (MMD). Elevation of the apparent diffusion coefficient (ADC) in normal-appearing white matter on conventional MRI may occur as a consequence of chronic haemodynamic failure. In the present study, the authors examined the relation of ADC with CVR and cognitive dysfunction in adults with MMD.</p>
</sec>
<sec><st>Methods</st>
<p>The authors measured ADC and CVR in the normal-appearing frontal white matter. CVR was calculated using dynamic susceptibility contrast-enhanced MRI and the acetazolamide challenge. A standardised and validated neuropsychological assessment test battery focusing on executive function was used.</p>
</sec>
<sec><st>Results</st>
<p>14 patients, 9 women and 5 men (mean age 36.6&plusmn;12.9&nbsp;years), were included. The authors found executive dysfunction in 7 of 13 tested patients. ADC and CVR were negatively correlated (Spearman coefficient: &ndash;0.46; p=0.015). Elevation of ADC predicted executive dysfunction (area under receiver operating characteristic curve (95% CI): 0.85 (0.59 to 1.16); p=0.032).</p>
</sec>
<sec><st>Conclusion</st>
<p>Elevation of ADC in the normal-appearing frontal white matter of adults with MMD was associated with reduced CVR and executive dysfunction. This preliminary study suggests that measurement of ADC might be used to detect patients at risk for cerebral ischaemia and cognitive impairment.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Calviere, L., Ssi Yan Kai, G., Catalaa, I., Marlats, F., Bonneville, F., Larrue, V.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301388</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301388</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Memory disorders (psychiatry), Radiology, Radiology (diagnostics)]]></dc:subject>
<dc:title><![CDATA[Executive dysfunction in adults with moyamoya disease is associated with increased diffusion in frontal white matter]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Cerebrovascular disease</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>591</prism:startingPage>
<prism:endingPage>593</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/594?rss=1">
<title><![CDATA[Construction and pilot assessment of the Upper Limb Assessment in Daily Living Scale]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/594?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>The upper limb function of hemiplegic patients is currently evaluated using scales that assess physical capacity or daily activities under test conditions. The present scale, the Upper Limb Assessment in Daily Living (ULADL) Scale, was developed to explore the subjective and objective functional capacities of such patients in a proximal to distal sequence.</p>
</sec>
<sec><st>Methods</st>
<p>A group of experts constructed a scale addressing 17 upper limb functions (five active passive and 12 active) which could be explored by a questionnaire (Q) and a test (T). Reproducibility, internal consistency, concurrent validity (Rivermead Motor Assessment (RMA)) and learning effect were estimated in a multicentre study.</p>
</sec>
<sec><st>Results</st>
<p>49 stroke patients were each rated three times within 7&nbsp;days by a total of 21 physicians, yielding a total of 142 ratings. The ULADL took 16&plusmn;8&nbsp;min to complete compared with 9&plusmn;5&nbsp;min for the RMA. Cronbach's alpha coefficient was 0.95 for Q and 0.97 for the practical tests (T). The global Q and T scores, and in particular the global Q score, were slightly higher at the second rating. The intra-rater intraclass correlation coefficient (ICC) was 0.65 (95% CI (0.44 to 0.79)) for Q and 0.97 (0.95 to 0.98) for T, and the inter-rater ICC was 0.95 for both Q and T. The Bland and Altman method showed good intra- and inter-rater reliability with no systematic trend. Correlation coefficients for ULADL versus RMA were &gt;0.80 for both Q and T.</p>
</sec>
<sec><st>Conclusions</st>
<p>The ULADL Scale has good psychometric properties and can explore patients with different degrees of upper limb impairment.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Rousseaux, M., Bonnin-Koang, H.-Y., Darne, B., Marque, P., Parratte, B., Schnitzler, A., Dehail, P., Bradai, N., Viton, J. M., Daveluy, W., Yelnik, A., Zadikian, M., Benaim, C.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-300929</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-300929</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Stroke]]></dc:subject>
<dc:title><![CDATA[Construction and pilot assessment of the Upper Limb Assessment in Daily Living Scale]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Cerebrovascular disease</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>594</prism:startingPage>
<prism:endingPage>600</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/601?rss=1">
<title><![CDATA[Mild cognitive impairment and cognitive-motor relationships in newly diagnosed drug-naive patients with Parkinson's disease]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/601?rss=1</link>
<description><![CDATA[
<sec><st>Background and aims</st>
<p>(1) To establish the prevalence of mild cognitive impairment (MCI) in newly diagnosed drug-naive patients with Parkinson's disease adopting recently proposed and more conservative preliminary research criteria. (2) To investigate the relation between cognitive performances, MCI and motor dysfunction.</p>
</sec>
<sec><st>Methods</st>
<p>132 consecutive newly diagnosed drug-naive PD patients and 100 healthy controls (HCs) underwent a neuropsychological evaluation covering different cognitive domains. Moreover, on the basis of the Unified Parkinson's Disease Rating Scale II/III, different motor scores were calculated and patients were classified in motor subtypes. 11 patients were excluded from the analysis during clinical follow-up which was continued at least 3&nbsp;years from the diagnosis; therefore, the final sample included 121 patients.</p>
</sec>
<sec><st>Results</st>
<p>MCI prevalence was higher in PD (14.8%) patients than in HCs (7.0%). PD patients reported lower cognitive performances than HCs in several cognitive domains; HCs also outperformed cognitively preserved PD patients in tasks of episodic verbal memory and in a screening task of executive functions. MCI-PD patients presented a more severe bradykinesia score than non-MCI PD patients and patients mainly characterised by tremor had better performances in some cognitive domains, and specific cognitive-motor relationships emerged.</p>
</sec>
<sec><st>Conclusions</st>
<p>Although the adoption of more conservative diagnostic criteria identified a lower MCI prevalence, we found evidence that newly diagnosed drug-naive PD patients present a higher risk of MCI in comparison with HCs. Axial symptoms and bradykinesia represent risk factors for MCI in PD patients and a classification of PD patients that highlights the presence/absence of tremor, as proposed in this study, is probably better tailored for the early stages of PD than classifications proposed for more advanced PD stages.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Poletti, M., Frosini, D., Pagni, C., Baldacci, F., Nicoletti, V., Tognoni, G., Lucetti, C., Del Dotto, P., Ceravolo, R., Bonuccelli, U.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301874</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301874</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: CNS (not psychiatric), Parkinson's disease, Memory disorders (psychiatry)]]></dc:subject>
<dc:title><![CDATA[Mild cognitive impairment and cognitive-motor relationships in newly diagnosed drug-naive patients with Parkinson's disease]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Movement disorders</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>601</prism:startingPage>
<prism:endingPage>606</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/607?rss=1">
<title><![CDATA[Ten year survival and outcomes in a prospective cohort of new onset Chinese Parkinson's disease patients]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/607?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>The 10 year outcomes and impact of motor and non-motor features on survival of a cohort of new onset Chinese Parkinson's disease (PD) patients were prospectively studied.</p>
</sec>
<sec><st>Method</st>
<p>A cohort of new onset PD patients from 1995 to 2002 was recruited from a regional hospital based movement disorder clinic. Subjects were classified into postural instability gait disorder (PIGD), tremor predominant type or mixed subtypes at presentation. All were evaluated yearly for development of sensory complaints, first significant fall, hallucinations, dementia, postural hypotension, speech disturbances, dysphagia and postural instability persisted during &lsquo;on&rsquo; medication state (PIPon). Mortality and predictors of death were determined.</p>
</sec>
<sec><st>Results</st>
<p>171 new onset PD patients were recruited. After a mean follow-up of 11.3&plusmn;2.6&nbsp;years, 50 (29%) patients died. The standardised mortality ratio was 1.1 (CI 0.8 to 1.5, p=0.34). 83 (49%) developed dementia, 81 (47%) had psychosis and 103 (60%) had sensory complaints. Postural hypotension was found in 58 (34%) patients, 108 (63%) had PIPon, 101 (59%) had falls, 102 (60%) had dysphagia, 148 (87%) had freezing of gait and 117 (68%) had speech disturbances. 46 (27%) were institutionalised whereas 54 (32%) lived independently. Dementia (HR 5.0, 95% CI 2.1 to 13.0), PIPon (HR 2.8, 95% CI 1.2 to 6.8), older onset (HR 1.05, 1&nbsp;year increase in age, 95% CI 1.0 to 1.1) and PIGD type (HR 2.1, 95% CI 1.2 to 3.7) were independent predictors of death.</p>
</sec>
<sec><st>Conclusions</st>
<p>10&nbsp;years into PD, a significant proportion of patients developed dopa resistant motor and non-motor features. Older onset, PIGD type, PIPon and dementia had a negative impact on survival. Standardised mortality ratio was 1.1.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Auyeung, M., Tsoi, T. H., Mok, V., Cheung, C. M., Lee, C. N., Li, R., Yeung, E.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301590</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301590</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Memory disorders (neurology), Drugs: CNS (not psychiatric), Parkinson's disease, Memory disorders (psychiatry), Psychotic disorders (incl schizophrenia)]]></dc:subject>
<dc:title><![CDATA[Ten year survival and outcomes in a prospective cohort of new onset Chinese Parkinson's disease patients]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Movement disorders</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>607</prism:startingPage>
<prism:endingPage>611</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/612?rss=1">
<title><![CDATA[Cognitive domains that predict time to diagnosis in prodromal Huntington disease]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/612?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Prodromal Huntington's disease (prHD) is associated with a myriad of cognitive changes but the domains that best predict time to clinical diagnosis have not been studied. This is a notable gap because some domains may be more sensitive to cognitive decline, which would inform clinical trials.</p>
</sec>
<sec><st>Objectives</st>
<p>The present study sought to characterise cognitive domains underlying a large test battery and for the first time, evaluate their ability to predict time to diagnosis.</p>
</sec>
<sec><st>Methods</st>
<p>Participants included gene negative and gene positive prHD participants who were enrolled in the PREDICT-HD study. The CAG&ndash;age product (CAP) score was the measure of an individual's genetic signature. A factor analysis of 18 tests was performed to identify sets of measures or latent factors that elucidated core constructs of tests. Factor scores were then fit to a survival model to evaluate their ability to predict time to diagnosis.</p>
</sec>
<sec><st>Results</st>
<p>Six factors were identified: (1) speed/inhibition, (2) verbal working memory, (3) motor planning/speed, (4) attention&ndash;information integration, (5) sensory&ndash;perceptual processing and (6) verbal learning/memory. Factor scores were sensitive to worsening of cognitive functioning in prHD, typically more so than performances on individual tests comprising the factors. Only the motor planning/speed and sensory&ndash;perceptual processing factors predicted time to diagnosis, after controlling for CAP scores and motor symptoms.</p>
</sec>
<sec><st>Conclusions</st>
<p>The results suggest that motor planning/speed and sensory&ndash;perceptual processing are important markers of disease prognosis. The findings also have implications for using composite indices of cognition in preventive Huntington's disease trials where they may be more sensitive than individual tests.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Harrington, D. L., Smith, M. M., Zhang, Y., Carlozzi, N. E., Paulsen, J. S., the PREDICT-HD Investigators of the Huntington Study Group]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301732</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301732</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Genetics, Movement disorders (other than Parkinsons), Memory disorders (psychiatry)]]></dc:subject>
<dc:title><![CDATA[Cognitive domains that predict time to diagnosis in prodromal Huntington disease]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Movement disorders</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>612</prism:startingPage>
<prism:endingPage>619</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/620?rss=1">
<title><![CDATA[Impact of DaTscan SPECT imaging on clinical management, diagnosis, confidence of diagnosis, quality of life, health resource use and safety in patients with clinically uncertain parkinsonian syndromes: a prospective 1-year follow-up of an open-label controlled study]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/620?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>This study assessed the impact of DaTscan on clinical management, diagnosis, confidence of diagnosis (CoD), quality of life (QoL), health resource use (HRU) and safety during a 1-year follow-up in patients with clinically uncertain parkinsonian syndromes (CUPS).</p>
</sec>
<sec><st>Methods</st>
<p>A total of 19 university hospital centres in Europe and the USA participated in this open-label, single-dose, prospective, clinical trial in patients with CUPS who were randomised to a DaTscan imaging group or to a no-imaging (control) group. The proportion of patients with changes in clinical management, diagnosis, CoD, QoL and HRU from baseline through 1&nbsp;year post-DaTscan was compared between groups.</p>
</sec>
<sec><st>Results</st>
<p>There were 273 patients randomised (135 DaTscan, 138 control). Significantly more patients in the DaTscan imaging group had at least one change in their actual clinical management after 12&nbsp;weeks (p=0.002) and after 1&nbsp;year (p&lt;0.001) compared with patients in the control group. In addition, significantly more DaTscan patients had changes in diagnosis and an increased CoD at 4&nbsp;weeks, 12&nbsp;weeks and 1&nbsp;year (all p&lt;0.001) compared with control patients. No significant differences in total score for QoL or HRU were observed between groups during the 1-year follow-up period. DaTscan was safe and well tolerated. One patient in the imaging group had an adverse event (headache) with suspected relationship to DaTscan post-administration.</p>
</sec>
<sec><st>Conclusions</st>
<p>DaTscan had a significant impact on clinical management, diagnosis and CoD in patients with CUPS. DaTscan is safe and well tolerated, and is a useful adjunct to differentiate a diagnosis of CUPS.</p>
</sec>
<sec><st>Trial registration number</st>
<p><A HREF="http://ClinicalTrials.gov">http://ClinicalTrials.gov</A> Identifier: NCT00382967.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kupsch, A. R., Bajaj, N., Weiland, F., Tartaglione, A., Klutmann, S., Buitendyk, M., Sherwin, P., Tate, A., Grachev, I. D.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301695</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301695</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Headache (including migraine), Pain (neurology), Parkinson's disease]]></dc:subject>
<dc:title><![CDATA[Impact of DaTscan SPECT imaging on clinical management, diagnosis, confidence of diagnosis, quality of life, health resource use and safety in patients with clinically uncertain parkinsonian syndromes: a prospective 1-year follow-up of an open-label controlled study]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Movement disorders</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>620</prism:startingPage>
<prism:endingPage>628</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/629?rss=1">
<title><![CDATA[Axonal integrity predicts cortical reorganisation following cervical injury]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/629?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Traumatic spinal cord injury (SCI) leads to disruption of axonal architecture and macroscopic tissue loss with impaired information flow between the brain and spinal cord&mdash;the presumed basis of ensuing clinical impairment.</p>
</sec>
<sec><st>Objective</st>
<p>The authors used a clinically viable, multimodal MRI protocol to quantify the axonal integrity of the cranial corticospinal tract (CST) and to establish how microstructural white matter changes in the CST are related to cross-sectional spinal cord area and cortical reorganisation of the sensorimotor system in subjects with traumatic SCI.</p>
</sec>
<sec><st>Methods</st>
<p>Nine volunteers with cervical injuries resulting in bilateral motor impairment and 14 control subjects were studied. The authors used diffusion tensor imaging to assess white matter integrity in the CST, T1-weighted imaging to measure cross-sectional spinal cord area and functional MRI to compare motor task-related brain activations. The relationships among microstructural, macrostructural and functional measures were assessed using regression analyses.</p>
</sec>
<sec><st>Results</st>
<p>Diffusion tensor imaging revealed significant differences in the CST of SCI subjects&mdash;compared with controls&mdash;in the pyramids, the internal capsule, the cerebral peduncle and the hand area. The microstructural white matter changes observed in the left pyramid predicted increased task-related responses in the left M1 leg area, while changes in the cerebral peduncle were predicted by reduced cord area.</p>
</sec>
<sec><st>Conclusion</st>
<p>The observed microstructural changes suggest trauma-related axonal degeneration and demyelination, which are related to cortical motor reorganisation and macrostructure. The extent of these changes may reflect the plasticity of motor pathways associated with cortical reorganisation. This clinically viable multimodal imaging approach is therefore appropriate for monitoring degeneration of central pathways and the evaluation of treatments targeting axonal repair in SCI.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Freund, P., Wheeler-Kingshott, C. A., Nagy, Z., Gorgoraptis, N., Weiskopf, N., Friston, K., Thompson, A. J., Hutton, C.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301875</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301875</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Unlocked, Neurological injury, Spinal cord, Trauma CNS / PNS, Trauma, Injury]]></dc:subject>
<dc:title><![CDATA[Axonal integrity predicts cortical reorganisation following cervical injury]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Spinal cord injury</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>629</prism:startingPage>
<prism:endingPage>637</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/638?rss=1">
<title><![CDATA[Central nervous system neuronal surface antibody associated syndromes: review and guidelines for recognition]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/638?rss=1</link>
<description><![CDATA[
<p>The concept of antibody mediated CNS disorders is relatively recent. The classical CNS paraneoplastic neurological syndromes are thought to be T cell mediated, and the onconeural antibodies merely biomarkers for the presence of the tumour. Thus it was thought that antibodies rarely, if ever, cause CNS disease. Over the past 10&nbsp;years, identification of autoimmune forms of encephalitis with antibodies against neuronal surface antigens, particularly the voltage gated potassium channel complex proteins or the glutamate N-methyl-D-aspartate receptor, have shown that CNS disorders, often without associated tumours, can be antibody mediated and benefit from immunomodulatory therapies. The clinical spectrum of these diseases is not yet fully explored, there may be others yet to be discovered and some types of more common disorders (eg, epilepsy or psychosis) may prove to have an autoimmune basis. Here, the known conditions associated with neuronal surface antibodies are briefly reviewed, some general aspects of these syndromes are considered and guidelines that could help in the recognition of further disorders are suggested.</p>
]]></description>
<dc:creator><![CDATA[Zuliani, L., Graus, F., Giometto, B., Bien, C., Vincent, A.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301237</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301237</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Unlocked, Editor's choice, Immunology (including allergy), Drugs: CNS (not psychiatric), Epilepsy and seizures, Infection (neurology), Psychotic disorders (incl schizophrenia)]]></dc:subject>
<dc:title><![CDATA[Central nervous system neuronal surface antibody associated syndromes: review and guidelines for recognition]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Neuro-immunology</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>638</prism:startingPage>
<prism:endingPage>645</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/646?rss=1">
<title><![CDATA[Relationship between movement disorders and obsessive-compulsive disorder: beyond the obsessive-compulsive-tic phenotype. A systematic review]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/646?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Obsessive&ndash;compulsive disorder (OCD) and symptoms (OC symptoms) are associated with tic disorders and share an aetiological relationship. The extent to which OCD/OC symptoms are correlated with other hyperkinetic movement disorders is unclear. The aim of this review was to investigate this co-occurrence and the extent to which OCD/OC symptoms and hyperkinetic movement disorders share a neurobiological basis.</p>
</sec>
<sec><st>Methods</st>
<p>A systematic review was performed, specifically searching for OCD/OC symptom comorbidity in hyperkinetic movement disorders using case control studies, longitudinal studies and family based studies. The literature search was conducted using PubMed and PsycINFO databases.</p>
</sec>
<sec><st>Results</st>
<p>Heterogeneity of measurement instruments to detect OCD diagnosis and OC symptoms decreased comparability between studies. The most convincing evidence for a relationship was found between the choreas (Huntington's disease and Sydenham's chorea) and OCD/OC symptoms. Furthermore, elevated frequencies of OC symptoms were found in small case control series of dystonias. Small family based studies in dystonia subtypes modestly suggest shared familial/genetic relationships between OC symptoms and dystonia.</p>
</sec>
<sec><st>Conclusion</st>
<p>Current data indicate a relationship between OCD/OC symptoms and the choreas. As OCD and the choreas have been associated with dysfunctional frontal&ndash;striatal circuits, the observed relationships might converge at the level of dysfunctions of these circuits. However, paucity of longitudinal and family studies hampers strong conclusions on the nature of the relationship.</p>
</sec>
<sec><st>Implications</st>
<p>The relationship between OCD and movement disorders needs further elaboration using larger family based longitudinal studies and sound instruments to characterise OC symptomatology. This could lead to better understanding of the shared pathology between OCD and hyperkinetic movement disorders.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fibbe, L. A., Cath, D. C., van den Heuvel, O. A., Veltman, D. J., Tijssen, M. A. J., van Balkom, A. J. L. M.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301752</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301752</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[JNNP Patients' choice, Genetics, Movement disorders (other than Parkinsons), Anxiety disorders (including OCD and PTSD)]]></dc:subject>
<dc:title><![CDATA[Relationship between movement disorders and obsessive-compulsive disorder: beyond the obsessive-compulsive-tic phenotype. A systematic review]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Neuropsychiatry</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>646</prism:startingPage>
<prism:endingPage>654</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/655?rss=1">
<title><![CDATA[Physiotherapists and patients with functional (psychogenic) motor symptoms: a survey of attitudes and interest]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/655?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Functional (psychogenic) motor symptoms are commonly encountered in clinical neurology. Physiotherapy has face validity as a treatment for such symptoms and, anecdotally, referral of patients with functional motor symptoms (FMS) to physiotherapy services is common practice by neurologists. Here the authors sought to explore exposure to and attitudes towards patients with FMS among neurophysiotherapists.</p>
</sec>
<sec><st>Method</st>
<p>The authors used an internet survey to gather information on the knowledge and attitudes of patients with FMS among 1402 members of a UK neurophysiotherapy organisation.</p>
</sec>
<sec><st>Results</st>
<p>The response rate was 61%. Most physiotherapists saw patients with FMS, and for 25% of respondents these patients made up over 10% of their workload. Respondents were moderately interested in treating these patients (ranking them sixth out of 10 neurological conditions), but had low self-judged knowledge. Most respondents felt physiotherapy had more to offer patients with FMS, but felt poorly supported by referring neurologists and by inadequate service structures.</p>
</sec>
<sec><st>Conclusions</st>
<p>Neurologists frequently refer patients with FMS to neurophysiotherapy services. Physiotherapists in general are interested in treating such patients and feel physiotherapy to be an appropriate treatment. However, inadequate service structures, knowledge and support from non-physiotherapy colleagues are judged to be barriers to provision of care.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Edwards, M. J., Stone, J., Nielsen, G.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-302147</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-302147</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Physiotherapy]]></dc:subject>
<dc:title><![CDATA[Physiotherapists and patients with functional (psychogenic) motor symptoms: a survey of attitudes and interest]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Neuropsychiatry</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>655</prism:startingPage>
<prism:endingPage>658</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/659?rss=1">
<title><![CDATA[Why are upper motor neuron signs difficult to elicit in amyotrophic lateral sclerosis?]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/659?rss=1</link>
<description><![CDATA[
<p>It is often difficult to identify signs of upper motor neuron lesion in the limbs of patients with amyotrophic lateral sclerosis, in whom there is neurogenic muscle wasting of varying severity. The reasons for this are complex and not related simply to the degree of lower motor neuron muscle wasting but, rather, depend on the pathophysiological abnormalities that develop in response to damage to descending motor pathways and to motor neurons and interneurons in the ventral horns of the spinal cord. The different mechanisms underlying the clinical phenomenology of the functional motor defect in amyotrophic lateral sclerosis, that lead to difficulty in detecting classical upper motor neuron signs, are discussed.</p>
]]></description>
<dc:creator><![CDATA[Swash, M.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2012-302315</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2012-302315</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Motor neurone disease, Neuromuscular disease, Spinal cord]]></dc:subject>
<dc:title><![CDATA[Why are upper motor neuron signs difficult to elicit in amyotrophic lateral sclerosis?]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Neurodegeneration</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>659</prism:startingPage>
<prism:endingPage>662</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/663?rss=1">
<title><![CDATA[Headache in three new cases of Harlequin syndrome with accompanying pharmacological comparison with migraine]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/663?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Harlequin syndrome (HS) is a rare autonomic disorder characterised by unilateral diminished sweating and flushing of the face in response to heat or exercise. Some patients with HS complain of headache.</p>
</sec>
<sec><st>Methods</st>
<p>We present three new cases to characterise their headache phenotype and pharmacology and review the literature of cases where headache was described.</p>
</sec>
<sec><st>Results</st>
<p>Two out of the three patients presented with episodes of unilateral headache associated with exercise: in one case the headache had migrainous features and was contralateral to the side where the flushing occurred, whereas the second patient, who had had migraine attacks in the past, had a brief throbbing headache, with no associated symptoms, ipsilateral to the facial flushing. The third woman had migraine but the attacks were not associated with HS. Pharmacological characterisation suggested the HS and migraine were biologically distinct. HS was not triggered by nitroglycerin and was unaffected by sumatriptan, dihydroergotamine and ergotamine. HS and migraine did not occur together. In the literature, we found six patients with both HS and headache, five of whom had migraine.</p>
</sec>
<sec><st>Conclusions</st>
<p>These data do not show any correlation between the phenotypic expression of migraine and HS suggesting the syndromes are pathogenetically independent.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Viana, M., Mathias, C. J., Goadsby, P. J.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-302124</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-302124</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Headache (including migraine), Pain (neurology)]]></dc:subject>
<dc:title><![CDATA[Headache in three new cases of Harlequin syndrome with accompanying pharmacological comparison with migraine]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Autonomic</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>663</prism:startingPage>
<prism:endingPage>665</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/666?rss=1">
<title><![CDATA[Cerebrovascular risk factors in early-onset dementia]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/666?rss=1</link>
<description><![CDATA[ <sec><st>Introduction</st> <p>Alzheimer's disease (AD) is the leading cause of dementia. Research into environmental factors is currently focused on cerebrovascular risk factors.<cross-ref type="bib" refid="b1">1</cross-ref> Treatment of vascular risk factors has been associated with slower cognitive decline and reduced risk of AD in older populations.<cross-ref type="bib" refid="b2">2</cross-ref> Genetics are important in rare genetically determined autosomal dominant familial patients with AD or frontotemporal dementia (FTD).<cross-ref type="bib" refid="b3">3</cross-ref> Apolipoprotein E (APOE) is a risk factor for familial late-onset sporadic AD, but its role as a risk factor in younger populations is unclear. The role of APOE as a risk factor for FTD is controversial.</p> <p>Early-onset dementia is dementia that develops in individuals prior to the age of 65&nbsp;years, and some studies suggest it is associated with a higher mortality. AD and FTD are the most common causes of dementia in this population.<cross-ref type="bib" refid="b4">4</cross-ref> The onset of FTD may be characterised by behavioural...]]></description>
<dc:creator><![CDATA[Atkins, E. R., Bulsara, M. K., Panegyres, P. K.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp.2009.202846</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp.2009.202846</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cerebrovascular risk factors in early-onset dementia]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>666</prism:startingPage>
<prism:endingPage>667</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/667?rss=1">
<title><![CDATA[Gluten-related recurrent peripheral facial palsy]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/667?rss=1</link>
<description><![CDATA[ <p>Recurrent peripheral facial paralysis (PFP) is an uncommon disorder that often occurs in the setting of family history. In 2001, we observed a patient with recurrent PFP who manifested symptoms of coeliac disease (CD) several months later. Because of this observation and because neurological disorders may be the only manifestation of atypical forms of CD,<cross-ref type="bib" refid="b1">1</cross-ref> we started to screen for gluten-related diseases all patients with at least two episodes of PFP who were referred to our department between 2001 and 2011. We performed initial screening serological tests (antigliadin, antitransglutaminase and antiendomysial antibodies), followed by a confirmatory small intestinal biopsy in positive cases. Testing for human leucocyte antigen (HLA) class 2 alleles was performed in patients with uncertain diagnosis<cross-ref type="bib" refid="b2">2</cross-ref> in that positive HLA-DQ2 or HLA-DQ8 genotypes are useful to support the diagnosis of potential CD in patients with positive serology and mild or absent histological lesions.<cross-ref...]]></description>
<dc:creator><![CDATA[Capone, F., Batocchi, A. P., Cammarota, G., Pilato, F., Profice, P., Di Lazzaro, V.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301921</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301921</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Gluten-related recurrent peripheral facial palsy]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>667</prism:startingPage>
<prism:endingPage>668</prism:endingPage>
</item>
<item rdf:about="http://jnnp.bmj.com/cgi/content/short/83/6/668?rss=1">
<title><![CDATA[A clinically silent, but severe, duodenal complication of duodopa infusion]]></title>
<link>http://jnnp.bmj.com/cgi/content/short/83/6/668?rss=1</link>
<description><![CDATA[ <p>Duodenal levodopa/carbidopa gel infusion (Duodopa) is an efficacious therapeutic strategy for motor and non-motor symptoms in advanced Parkinson's disease (PD).<cross-ref type="bib" refid="b1">1&ndash;3</cross-ref><cross-ref type="bib" refid="b2"></cross-ref><cross-ref type="bib" refid="b3"></cross-ref> Technical issues like kinking, knotting or obstruction of the tube are frequent, as well as complications due to the procedure, such as buried bumper syndrome, local infection and dislocation of the tube in the stomach (57%&ndash;69% of the patients), but they are seldom associated with severe adverse effects.<cross-ref type="bib" refid="b1">1</cross-ref> <cross-ref type="bib" refid="b3">3</cross-ref> <cross-ref type="bib" refid="b4">4</cross-ref> In most cases, they are generally easy to suspect due to the immediate lack of therapeutic efficacy or malfunction of the infusion pump. We describe a rare and very serious gut complication associated with the device, which is difficult to recognise because of the persistence of clinical benefit on motor signs.</p> <p>A 72-year-old man with a medical history of hypertension and chronic obstructive pulmonary disease, and with...]]></description>
<dc:creator><![CDATA[Bianco, G., Vuolo, G., Ulivelli, M., Bartalini, S., Chieca, R., Rossi, A., Rossi, S.]]></dc:creator>
<dc:date>2012-05-08T18:44:42-07:00</dc:date>
<dc:identifier>info:doi/10.1136/jnnp-2011-301984</dc:identifier>
<dc:identifier>hwp:master-id:jnnp;jnnp-2011-301984</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A clinically silent, but severe, duodenal complication of duodopa infusion]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>83</prism:volume>
<prism:number>6</prism:number>
<prism:startingPage>668</prism:startingPage>
<prism:endingPage>670</prism:endingPage>
</item>
</rdf:RDF>
