User:Shibley Rahman

Please note that this is an entirely autobiographical account, written by Dr. Shibley Rahman

Introduction

Shibley Rahman is a distance learning teacher. He is not a professional academic, but he does have recognised expertise in the cognitive neuropsychology of neurodegeneration. He combines this with his other interests in law, entrepreneurship, and raising awareness of disability issues.

Early life and education Dr Shibley Rahman QS MA MB BChir PhD MRCP(UK) LLB(Hons) FRSA MSB (born 18 June 1974) is a British academic, neuroscientist and entrepreneur, born in the Queen Mother's Hospital in Glasgow. His parents are both Bengali; his father is a retired successful general practitioner, having practised near Brighton for nearly thirty years. He lives alone in the village of Primrose Hill, North London, and has no children. He originally went to Cumnor House School, Danehill, East Sussex, previous other alumni including Nigel Lawson (Baron Lawson of Blaby), the former Tory Chancellor of the Exchequer.

Shibley Rahman was then awarded as a prestigious Queen's Scholar at Westminster School, London, on the basis of a competitive entrance examination known as "The Challenge" in May 1987. He was approximate contemporaries with leading entrepreneur and businessperson Martha Lane Fox, and BBC Foreign Affairs Correspondent James Reynolds, and Dido (singer); and honorary scholars award-winning writer and translator Daniel Hahn and profilic economist and journalist Philippe Legrain; Having achieved four grade As in mathematics, further mathematics, chemistry and physics, all at GCE Advanced Level and two grade 1s in the Special Paper at Advanced Level, he then worked briefly in a vacation job at the Royal Institution of Great Britain in a junior research role involving superconductivity, having been awarded a Laura Ashley studentship.

On completing his schooling at Westminster School, Shibley Rahman went to the University of Cambridge in the Michaelmas Term 1993. There, he studied the Medical and Veterinary Sciences Tripos, and was awarded the second highest first class honours degree mark in his Bachelor of Arts in neuroscience in the Natural Sciences Tripos, 1996. He was awarded a foundation scholarship by his college, Jesus College, Cambridge. For his finals, he was supervised by Professor Simon Baron-Cohen, from Trinity College, Cambridge. His dissertation was on the inheritance of synaesthesia. Shibley Rahman completed his medical training at Cambridge, graduating in 2001 having done the M.B./Ph.D. course at Cambridge, and his doctor of philosophy on specific cognitive deficits in the frontal dementias was conferred by the University of Cambridge without corrections, also in 2001. He passed the Membership Examination through the Royal College of Physicians of Edinburgh, the Royal College of Physicians and Surgeons of Glasgow and the Royal College of Physicians of London in April 2005,[1] and become an Advanced Life Support provider in cardiac arrests in August 2003.

Shibley Rahman is reported to have been suffering from an alcohol dependence syndrome between approximately approximately 2003 and June 3rd 2007. He blogs regularly [1, 2]. He was in a coma on the intensive care unit due to a clinically proven diagnosis of meningitis for two months in 2007, having been successfully resuscitated by a trust in London from a cardiac arrest [3], and has been then been fully in recovery from alcoholism since that episode [4]. Since 2007, he has been disabled, but, even while recovering in hospital, he completed his Graduate Diploma in Law (postgraduate certificate in the law) at BPP Law School in London, and was subsequently awarded his Bachelor of Laws there. He is currently a part-time distance learning student of the Master of Laws at the College of Law of England and Wales, where he has specialised in commercial law. Shibley Rahman's interests have subsequently developed as being wide-ranging, encompassing a diverse range of issues in general medicine, law, ethics and neuroethics. Shibley Rahman has been a member of the World Neuroethics Society since early 2010.

Professional life Shibley Rahman became elected to a Fellowship of the Royal Society for the Encouragement in the Arts, Commerce and Entrepreneurship in 2010, where he participates in the Social Brain project on the basis of his research in social neuroscience. [5] Secondly he has also been elected elected to membership of the Society of Biology, where all members have to hold a postgraduate degree in a biological science, and be able to demonstrate a commitment to furthering the biological sciences. Shibley Rahman has written two books on postgraduate medical education [6][7], and is passionate about medical and legal e-learning, being a company director of an internet-based education company [8]. He is an associate member of the Institute of Directors, and is a registered and qualified PRINCE2 complex project management practitioner. PRINCE2 is a systematic mechanism used by many project managers for managing a complex project in a controlled environment. He is also active in medical journalism, being a member of the European Medical Writers' Association. Between 2008-present day, he has applied his academic knowledge and skills in medical research for charities, both in doing pro bono charity work and as a paid consultant, in both cases providing actual expertise in 'niche' academic medical subject areas [9].

Specific contribution to the cognitive neuropsychology of neurodegeneration Dementia (including the behavioural variant of frontotemporal dementia) There are various types of subtypes of FTD described commonly in the literature: see the page on frontotemporal dementia. However, the key interest of Shibley Rahman from his research studies at Cambridge has been the behavioural variant of frontotemporal dementia. His very highly cited paper internationally (it currently has close to 250 citations on Google Scholar) [10] introduced evidence that a major area of pathology early in behavioural variant frontotemporal dementia ("bvFTD"), and this study has engaged dementia experts throughout the world in the last decade. Shibley Rahman and colleagues hypothesised that the major locus of dysfunction in bvFTD was located in a part of the prefrontal cortex called the ventromedial prefrontal cortex [11], accounting for the remarkable clinical presentation of patients in their early course of the disease. It is this paper (and a few other studies not described in this article) which formed the core focus of this doctoral thesis which was awarded by the University of Cambridge in 2001 [12].

Very many commentators had observed that one of the most commonly used screening test in dementia, the Folstein Mini Mental State Examination (MMSE), tended to prove unreliable for the detection and monitoring of patients with bvFTD. They tended frequently perform normally even when requiring nursing home care treatment [13]. At the time of the research undertaken by Shibley Rahman and colleagues at Cambridge, patients with a queried diagnosis of early bvFTD were attending the memory clinic worldwide, with profound changes in personality and behaviour, and yet performing adequately on ‘frontal lobe tests’. It had long been recognized that the prefrontal cortex is involved in various different corticostriatal loops [14]. The performance on frontal lobe tests, typically highly sensitive to intact dorsolateral prefrontal cortex, of early bvFTD patients can be highly variable [15].

Shibley Rahman and colleagues used a decision-making paradigm similar to the Iowa Gambling Task, originally developed by Antoine Bechara and António Damásio. In the Brain study, patients with frontal dementia were found to show genuine risk-taking behaviour with increased deliberation times rather than merely impulsive behaviour. Given the nature of the cognitive deficits demonstrated by these patients, the authors postulated that relatively early in the course of the disease the ventromedial cortex was a major locus of dysfunction, and that this would most likely relate to the behavioural presentation of these patients clinically described in the individual case histories. The finding has been subsequently been supported by neuroimaging [16]. The importance of identifying such cognitive deficits in bvFTD precisely has been in a better formulation of the international consensus criteria for frontotemporal dementia , and has been acknowledged accordingly by many separate international researcher groups [17]. The finding is widely referred to in key texts for specialists in dementia research, as well as being cited in one of the world's leading general medical textbooks, as a key reading for a general physician who wishes to learn about dementia.[18] The involvement of the ventromedial prefrontal cortex in bvFTD has latterly further been explained in a wide range of different contexts in the popular press, including morality [19], impaired recognition of sarcasm [20], and pathological gambling. [21]

The published research has had a part in influencing the research into bvFTD in the last decade in two major ways. Firstly, there has been a widespread appreciation, particularly in the (peer-reviewed) published research from outside Cambridge, of the critical need for everyday tests used in clinical practice to ‘tap’ the right domain of frontal lobe function in this way In the context of the frontal lobe dementias [22] [23]. There are, however, significant methodological considerations, in extrapolating the findings from this very small sample to a larger sample of patients with bvFTD. For example, the ante-mortem diagnosis of frontotemporal dementia, compared to the gold standard of post-mortem diagnosis, has previously been described as 'moderately sensitive' by one prominent group of researchers. However, as described above, other evidence can be interpreted as highly supportive of the hypothesis. The findings in relation to the functions of the frontal lobes generally have been exhaustively reviewed [24] [25] [26] [27] [28] [29]. The group of Prof. Bruce Miller, Clinical Director of the UCSF Memory and Aging Center in California USA has extensively reviewed the behavioural and psycholgoical changes that appear to be pursuant to atrophy of the ventromedial prefrontal (and closely-related orbitofrontal) cortex, and have recently even hypothesised that the phylogenetically new neurons found in this region, called von Economo neurons, may be selectively vulnerable in bvFTD. [30]

Secondly, the group at Cambridge investigated two possible psychopharmacological interventions in bvFTD; methylphenidate [31], the "methylphenidate study") and paroxetine [32], (the "paroxetine study"). The studies have also played a small part in contributing to a discussion as to the role of the central neurotransmitter systems in cognition; for example, in a wide-ranging review, Schmitt et al. (2006) considered the meaning of the results from the paroxetine study in our understanding of serotonin in human brains. [33] However, arguably, a material impact of the work from the methylphenidate study and the paroxetine study has been, various groups have argued, in sustained international efforts to understand how the neurotransmitter systems in FTD can be modulated rationally.

Studies of neurotransmitter deficiencies in frontotemporal dementia (FTD) can be helpful in developing treatments [34]. Treatment studies on FTD are scarce, given the prevalence and severity of this illness. Larger, well-controlled treatment studies are required to reach more definitive conclusions about treatment efficacy. Multicentre studies are likely the best way to complete treatment studies in a timely manner. [35] This approach has been fully embraced by many other international research groups as part of their research programmes into dementia, citing and discussing in their published reviews the results above in their contributions. [35][36][37] As a response to these limited studies, it has now been recommended that experts in FTD arrive at a consensus to define standards for all clinical trials in FTD, citing these studies on paroxetine and ritaiin, and that such studies should include standards for diagnostic criteria, tests of severity, experimental design, and outcome measures; the article by Prof. Morris Freedman (2007), from the Baycrest Centre for Geriatric Care in the University of Toronto, Canda, considered these studies, and gave valued judgments to the international community on how best to progress with psychopharmacological studies in dementia [38] There is much work to be done in the future: for example, methylphenidate has been recently proposed by Dolder and colleagues (2010) as possible treatment for apathy in patients with dementia, compared to other psychostimulants [39]. There has been a relative paucity of drug studies in dementia. In summary, the general consensus of the global dementia research community is that, at this present time, rigorous trials of medications are needed to reconcile what has been considered to be a mismatch between good evidence-based medicine and what clinicians do in practice; a recent independent systematic review of the few number of few trials involving SSRIs (including the paroxetine study above), conducted in Canada, concluded that, "although there is evidence to support a serotonergic deficit, and clinicians frequently prescribe selective serotonin reuptake inhibitors to patients with FTD, only paroxetine and trazodone have been studied." [40]

Idiopathic Parkinson's disease: freezing-of-gait and quality-of-life Freezing-of-gait/festination of gait is a significant early phenomenon in Parkinson's disease. Whilst as a post-doctoral student at the Institute of Neurology at Queen Square, London, part of the UCL (University College, London), Shibley published two important papers based on a questionnaire survey of patients with idiopathic Parkinson's disease. In the first study, the "freezing study", a number of factors were identified could specifically tend to cause or ameliorate the phenomenon of "freezing" in this condition [41]. It was noted that the factors that commonly induced freezing-of-gait were, in fact, turning, fatigue, confined spaces and stressful situations, in addition to emotional factors. In contrast, freezing-of-gait was also ameliorated by various attentional and external cueing strategies. However, it should be noted that the size of the sample was relatively small. It is particularly noteworthy not all groups have been able to observe exactly the same pattern of results as in the questionnaire study described here, but they have explicitly addressed the findings from the questionnaire study and offered alternative explanations for the results which they have found from their studies, conducted elsewhere [42][43].

However, in many of the studies, there has been an emergent consensus to identify the factors which can cause patients to 'unfreeze' through the phenomenon known as 'paradoxical kinesia' [44]. In an academic discussion on the subject, Dr. Friedrich Asmus and colleagues (2009) from the University of Tübingen, Germany, offered that, on the basis of the freezing study above, that, "in this context, visual cueing has a pivotal role, as shown by the report of a patient with PD during the war who was paradoxically able to run by following the footsteps of his wife in front of him. Smilar and reproducible effects of patterned movements like running stairs have been described in the context of paradoxical kinesis" [45] Another finding from the freezing study was that patients with Parkinson's disease reported that turning difficulties appeared to be associated with freezing, but the problem was that only limited studies had been conducted to characterize these difficulties. In a formal analysis, the laboratory of Prof. Alice Nieuwboer at the University of Leuven in Belgoum indeed this report to be borne out in formal gait analysis, and further found that, during turning, non-freezers and controls decreased their cadence whereas freezers increased it, which may be related to freezing-of-gait [46].

In a different study, the "quality-of-life study", it emerged the quality-of-life in patients with Parkinson's disease tended to be heavily influenced by certain factors above others [47]. This concept was not at all new in the literature. However, in that particular study, in addition to depression and anxiety, the major predictors of quality-of-life were found to be shuffling, difficulty turning, falls, difficulty in dressing, fatigue, confusion, autonomic disturbance particularly urinary incontinence, unpredictable on/off fluctuations, and sensory symptoms such as pain. The study is entirely in keeping with the huge body of literature which have emphasised the importance of psychological factors such as anxiety and depression in the quality-of-life of patients with Parkinson’s disease [48] [49] [50]. Independent commentators have generally opined that it has been useful to consider the ‘relative’ importance of symptoms for patients; results from this study have been used by to argue some of these factors have been traditionally underestimated, such as fatigue, but are actually extremely important [51]. A major criticism of this study is that no questions about social factors were included. In future research, the relative importance of clinical and social factors, for example the level of social support, in quality-of-life will have to be better elucidated. It has been argued recently that, on the basis of a large recent cross-sectional study, the quality-of-life of patients with Parkinson’s disease in Western countries is predominately affected by clinical parameters, but this is not the case for Eastern European countries [52].

Personal interests Shibley Rahman is active on the social media as a known supporter of the UK Labour Party, and takes part occasionally in internet debates.[53] He was rendered physically disabled after his meningitis in 2007 [54], and campaigns actively on raising awareness of general disability issues.[55]


References 1 http://docserver.ingentaconnect.com/deliver/connect/rcop/14702118/v5n4/s27.pdf?expires=1282963654&id=58369026&titleid=5200003&accname=Guest+User&checksum=9BABC762563B1DAA1B32A14779281170


2 http://shibleyrahman.com


3 http://www.shibleyrahman.com


4 http://www.naymz.com/shibley_rahman


5 Meeting of the British Neuropsychiatric Association at the Royal Society, London (13 January 2000): "The Social Brain" : www.bnpa.org.uk/2000%20PRO.doc


6 Best of Five MRCP2 Practice Questions – with explanatory answers”, authors: Shibley Rahman and Avinash Sharma (published by Radcliffe Press, September 2009) ISBN 978-1846193606


7 Revision Notes for MRCP Part 2 PACES”, authors: Shibley Rahman and Avinash Sharma. Jaypee Publishers London, September 2010.


8 http://www.lawandmedicine.org.uk/User/AboutUs.aspx


9 http://www.linkedin.com/in/drshibleyrahman/


10 http://brain.oxfordjournals.org/cgi/content/abstract/122/8/1469


11 Rahman, S., Sahakian, B.J., Hodges, J.R., Rogers, R.D., Robbins, T.W. (1999) Specific cognitive deficits in early behavioural variant frontotemporal dementia. Brain 122 (Pt 8):1469-93


12 Shibley Rahman. Ph.D. thesis, examined and conferred by the University of Cambridge (Cambridge, UK): "Specific cognitive deficits in the frontal lobe dementias">


13 Weder ND, Aziz R, Wilkins K, Tampi RR. Frontotemporal dementias: a review. [Review.] Ann Gen Psychiatry. 2007 Jun 12;6:15.


14 Cummings JL. Frontal-subcortical circuits and human behaviour. [Review.] Arch Neurol 1993; 50: 873-80.


15 Hornberger M, Shelley BP, Kipps CM, Piguet O, Hodges JR. Can progressive and non-progressive behavioural variant frontotemporal dementia be distinguished at presentation? J Neurol Neurosurg Psychiatry. 2009 Jun;80(6):591-3. Epub 2009 Feb 18.


16 Perry RJ, Graham A, Williams G, Rosen H, Erzinçlioglu S, Weiner M, Miller B, Hodges J. Patterns of Frontal Lobe Atrophy in Frontotemporal Dementia: A Volumetric MRI Study. Dement Geriatr Cogn Disord 2006;22:278-287 (DOI: 10.1159/000095128 http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=DEM2006022004278)


17 MF Mendez and KM Perryman. Neuropsychiatric Features of Frontotemporal Dementia Evaluation of Consensus Criteria and Review. [Review.] Neuropsychiatry Clin Neurosci 2002;14:424-429, : http://neuro.psychiatryonline.org/cgi/reprint/14/4/424


18 JR Hodges. Chapter 24.2: Dementia. [Review.] In "Oxford Textbook of Medicine", ed. DA Warrell, TM Cox, JD Firth. Oxford University Press, Oxford UK http://otm.oxfordmedicine.com/cgi/content/full/5/1/med-9780199204854-chapter-2442.


19 "I didn't sin: it wasn't my brain (a commnentary on morality," (A commentary on the FTD and the ventromedial prefrontal cortex in moral decisions) http://www.neuroquantology.com/repository/index.php?option=com_content&view=article&id=111:i-didnt-sinit-was-my-brain&catid=99:free-will&Itemid=72


20 http://www.alzheimers.org.au/upload/DementiaNews23Jan09.pdf

21 http://www.medscape.com/viewarticle/724017_3


22 Bechara, A; Damasio, H; Tranel, D; & Anderson, SW; (1998). "Dissociation Of Working Memory from Decision Making within the Human Prefrontal Cortex". Journal of Neuroscience 18 (1): 428–437. PMID 9412519.


23 Storey, E. The frontal dementias. [Review.] Neurology Asia 2004; 9 : 11 – 20. J Cogn Neurosci. 2004 Jan-Feb;16(1):74-89. http://www.neurology-asia.org/articles/20042_011.pdf


24 Gomez-Beldarrain M, Harries C, Garcia-Monco JC, Ballus E, Grafman J. Patients with right frontal lesions are unable to assess and use advice to make predictive judgments. J Cogn Neurosci. 2004 Jan-Feb;16(1):74-89.


25 Knopman DS, Boeve BF, Parisi JE, Dickson DW, Smith GE, Ivnik RJ, Josephs KA, Petersen RC. Antemortem diagnosis of frontotemporal lobar degeneration. Ann Neurol. 2005 Apr;57(4):480-8.


26 AR Damasio, SW Anderson (1985, later revision) The frontal lobes [Review.] http://www.books.google.com


27 J Blair, DR Mitchell, K Blair (2005) The psychopath: Emotion and the brain [Review.] http://www.books.google.com


28 PF Malloy, ED Richardson (1994). Assessment of frontal lobe functions [Review.] J Neuropsychiatry Clin Neurosci 1994; 6:399-410


29 Gluck MA, Poldrack RA, Kéri S. The cognitive neuroscience of category learning. [Review.] Neurosci Biobehav Rev. 2008;32(2):193-6. Epub 2007 Nov 22.


30 Viskontas IV, Possin KL, Miller BL. Symptoms of frontotemporal dementia provide insights into orbitofrontal cortex function and social behavior. [Review;] Ann N Y Acad Sci. 2007 Dec;1121:528-45. Epub 2007 Sep 10.


31 Rahman, S., Sahakian, B.J., Nestor, P.J., Hodges, J.R., Robbins, T.W. Methylphenidate ('Ritalin') can Ameliorate Abnormal Risk-Taking Behavior in the Frontal Variant of Frontotemporal Dementia. Nature (Neuropsychopharmacology). 2005 Sep 7; [Epub ahead of print]


32 Deakin, J., Rahman, S., Sahakian, B.J., Nestor, P.J., Hodges, J.R., Robbins, T.W. Paroxetine does not improve symptoms and impairs cognition in frontotemporal dementia: a double-blind randomized controlled trial. Psychopharmacology (Berl). 2004 Apr;172(4):400-8. Epub 2003 Dec 10.


33 Schmitt JA, Wingen M, Ramaekers JG, Evers EA, Riedel WJ. Serotonin and human cognitive performance. [Review.] Curr Pharm Des. 2006;12(20):2473-86.


34 Huey ED, Putnam KT, Grafman J. A systematic review of neurotransmitter deficits and treatments in frontotemporal dementia. [Review.] Neurology. 2006 Jan 10;66(1):17-22.


35 Frontotemporal Dementia in Older Adults: Diagnostic and Therapeutic Challenges . Clinical geriatrics. Volume 17(1), January 2009. http://www.clinicalgeriatrics.com/articles/Frontotemporal-Dementia-Older-Adults-Diagnostic-and-Therapeutic-Challenges.


36 Kaye ED, Petrovic-Poljak A, Verhoeff NP, Freedman M. Frontotemporal Dementia and Pharmacologic Interventions. [Review.] J Neuropsychiatry Clin Neurosci.2010; 22: 19-29. http://neuro.psychiatryonline.org/cgi/content/abstract/22/1/19


37. Erik D. Roberson Frontotemporal dementia. [Review.] Current neurology and neuroscience reports. Volume 6, Number 6, 481-489, DOI: 10.1007/s11910-006-0050-7 http://www.springerlink.com/content/p53018561n15977x/


38. Freedman M. Frontotemporal dementia: recommendations for therapeutic studies, designs, and approaches. Can J Neurol Sci. 2007 Mar;34 Suppl 1:S118-24.


39. Dolder CR, Davis LN, McKinsey J. Use of Psychostimulants in Patients with Dementia (October) [Review.] Ann Pharmacother. 2010 Aug 24. [Epub ahead of print]


40. Chow TW. Treatment approaches to symptoms associated with frontotemporal degeneration. [Review.] Curr Psychiatry Rep. 2005 Oct;7(5):376-80.>


41. Rahman, S., Griffin, H.J., Quinn, N.P., Jahanshahi, M. The factors that induce or overcome freezing. Behav. Neurol. 2008;19(3):127-36.


42. Hausdorff JM. Gait dynamics in Parkinson's disease: common and distinct behavior among stride length, gait variability, and fractal-like scaling. Chaos. 2009 Jun;19(2):026113.


43. Ziegler K, Schroeteler F, Ceballos-Baumann AO, Fietzek UM. A new rating instrument to assess festination and freezing gait in Parkinsonian patients. Mov Disord. 2010 Jun 15;25(8):1012-8.


44. Schlesinger I, Erikh I, Yarnitsky D. Paradoxical kinesia at war. [Review.] Mov Disord. 2007 Dec;22(16):2394-7.


45. Robottom BJ, Weiner WJ, Asmus F, Huber H, Gasser T, Schöls L. Kick and rush: paradoxical kinesia in Parkinson disease. Neurology. 2009 Jul 28;73(4):328; author reply 328-9.


46. Spildooren J, Vercruysse S, Desloovere K, Vandenberghe W, Kerckhofs E, Nieuwboer A. Freezing of gait in Parkinson's disease: The impact of dual-tasking and turning. Mov Disord. 2010 Jul 14. [Epub ahead of print]


47. Rahman, S., Griffin, H.J., Quinn, N.P., Jahanshahi, M. Quality of life: the relative contribution of physical symptoms. Mov Disord. 2008 Jul 30;23(10):1428-34


48. Quelhas R, Costa M. Anxiety, depression, and quality of life in Parkinson's disease. J Neuropsychiatry Clin Neurosci. 2009 Fall;21(4):413-9.


49. Aarsland D, Pedersen KF, Ehrt U, Bronnick K, Gjerstad MD, Larsen JP. [Neuropsychiatric and cognitive symptoms in Parkinson disease] [Article in Norwegian] [Review.] Tidsskr Nor Laegeforen. 2008 Sep 25;128(18):2072-6.


50. Montel S, Bonnet AM, Bungener C. Quality of life in relation to mood, coping strategies, and dyskinesia in Parkinson's disease. J Geriatr Psychiatry Neurol. 2009 Jun;22(2):95-102. Epub 2009 Jan 15.


51. Levine J, Greenwald BD Fatigue in Parkinson disease, stroke, and traumatic brain injury. [Review.] Phys Med Rehabil Clin N Am. 2009 May;20(2):347-61. http://www.integraronline.com.br/admin/download/20100222155153.pdf


52. Winter Y, von Campenhausen S, Popov G, Reese JP, Balzer-Geldsetzer M, Kukshina A, 45. Zhukova TV, Bertschi N, Bötzel K, Gusev E, Oertel WH, Dodel R, Guekht A. Social and clinical determinants of quality of life in Parkinson's disease in a Russian cohort study. Parkinsonism Relat Disord. 2010 May;16(4):243-8. Epub 2009 Dec 21.


53. http://www.labourlist.org/andrew-ranwnsley-serialisation-observer-end-of-party


54. http://shibleyrahman.gather.com/


55. http://www.disaboomlive.com/Blogs/shibleyrahman/Default.aspx



--Entrepreneur 09:07, 29 August 2010 (PDT)