Alexandra Sinclair

Dr. Alexandra Sinclair


Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 June 2021 in Nature Reviews Neurology
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AEAnna K. Eigenbrodt
Anna K. Eigenbrodt
HAHåkan Ashina
Håkan Ashina
SKSabrina Khan
Sabrina Khan
HDHans-Christoph Diener
Hans-Christoph Diener
DMDimos D. Mitsikostas
Dimos D. Mitsikostas
MAMessoud Ashina
Messoud Ashina
Migraine is a disabling primary headache disorder that directly affects more than one billion people worldwide. Despite its widespread prevalence, migraine remains under-diagnosed and under-treated. To support clinical decision-making, we convened a European panel of experts to develop a ten-step approach to the diagnosis and management of migraine. Each step was established by expert consensus and supported by a review of current literature, and the Consensus Statement is endorsed by the European Headache Federation and the European Academy of Neurology. In this Consensus Statement, we introduce typical clinical features, diagnostic criteria and differential diagnoses of migraine. We then emphasize the value of patient centricity and patient education to ensure treatment adherence and satisfaction with care provision. Further, we outline best practices for acute and preventive treatment of migraine in various patient populations, including adults, children and adolescents, pregnant and breastfeeding women, and older people. In addition, we provide recommendations for evaluating treatment response and managing treatment failure. Lastly, we discuss the management of complications and comorbidities as well as the importance of planning long-term follow-up.

1 January 2016 in The Lancet Neurology
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Journal Article
Closed access
KMKeira A Markey
Keira A Markey
SMSusan P Mollan
Susan P Mollan
RJRigmor H Jensen
Rigmor H Jensen
ASAlexandra Sinclair
Alexandra Sinclair

7 July 2010 in BMJ
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Journal Article
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ASAlexandra Sinclair
Alexandra Sinclair
MBM. A. Burdon
M. A. Burdon
PNPeter G Nightingale
Peter G Nightingale
ABAlexandra K Ball
Alexandra K Ball
PGPeter Good
Peter Good
SRSaaeha Rauz
Saaeha Rauz
Objective To observe intracranial pressure in women with idiopathic intracranial hypertension who follow a low energy diet. Design Prospective cohort study. Setting Outpatient department and the clinical research facility based at two separate hospitals within the United Kingdom. Participants 25 women with body mass index (BMI) >25, with active (papilloedema and intracranial pressure >25 cm H2O), chronic (over three months) idiopathic intracranial hypertension. Women who had undergone surgery to treat idiopathic intracranial hypertension were excluded. Intervention Stage 1: no new intervention; stage 2: nutritionally complete low energy (calorie) diet (1777 kJ/day (425 kcal/day)); stage 3: follow-up period after the diet. Each stage lasted three months. Main outcome measure The primary outcome was reduction in intracranial pressure after the diet. Secondary measures included score on headache impact test-6, papilloedema (as measured by ultrasonography of the elevation of the optic disc and diameter of the nerve sheath, together with thickness of the peripapillary retina measured by optical coherence tomography), mean deviation of Humphrey visual field, LogMAR visual acuity, and symptoms. Outcome measures were assessed at baseline and three, six, and nine months. Lumbar puncture, to quantify intracranial pressure, was measured at baseline and three and six months. Results All variables remained stable over stage 1. During stage 2, there were significant reductions in weight (mean 15.7 (SD 8.0) kg, P<0.001), intracranial pressure (mean 8.0 (SD 4.2) cm H2O, P<0.001), score on headache impact test (7.6 (SD 10.1), P=0.004), and papilloedema (optic disc elevation (mean 0.15 (SD 0.23) mm, P=0.002), diameter of the nerve sheath (mean 0.7 (SD 0.8) mm, P=0.004), and thickness of the peripapillary retina (mean 25.7 (SD 36.1) µ, P=0.001)). Mean deviation of the Humphrey visual field remained stable, and in only five patients, the LogMAR visual acuity improved by one line. Fewer women reported symptoms including tinnitus, diplopia, and obscurations (10 v 4, P=0.004; 7 v 0, P=0.008; and 4 v 0, P=0.025, respectively). Re-evaluation at three months after the diet showed no significant change in weight (0.21 (SD 6.8) kg), and all outcome measures were maintained. Conclusion Women with idiopathic intracranial hypertension who followed a low energy diet for three months had significantly reduced intracranial pressure compared with pressure measured in the three months before the diet, as well as improved symptoms and reduced papilloedema. These reductions persisted for three months after they stopped the diet.

17 February 2016 in Journal of Neurology, Neurosurgery & Psychiatry
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SMSusan P Mollan
Susan P Mollan
FAFizzah Ali
Fizzah Ali
GHGhaniah Hassan-Smith
Ghaniah Hassan-Smith
HBHannah Botfield
Hannah Botfield
DFDeborah I Friedman
Deborah I Friedman
ASAlexandra Sinclair
Alexandra Sinclair
Idiopathic intracranial hypertension (IIH) is a rare but important disease associated with significant morbidity. There is an expected rise in prevalence in line with the escalating global burden of obesity. Modern revisions in the terminology and diagnostic criteria for IIH help guide clinicians in investigations and researchers in standardising recruitment criteria for clinical trials. The pathophysiology of IIH is incompletely characterised; suggested underpinning mechanisms include the role of cerebrospinal fluid regulation as well as metabolic and endocrinological perspectives. Recent treatment trials are providing insights into the management but debate still surrounds key areas in treatment. This review will provide an up-to-date discussion on the potential pathogenic mechanisms and management of IIH.

26 January 2012 in Journal of Neurology
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BWBen L. C. Wright
Ben L. C. Wright
JLJames T. F. Lai
James T. F. Lai
ASAlexandra Sinclair
Alexandra Sinclair

1 August 2013 in Endocrine Reviews
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LGLaura L. Gathercole
Laura L. Gathercole
GLGareth G. Lavery
Gareth G. Lavery
SMStuart A. Morgan
Stuart A. Morgan
MCMark S. Cooper
Mark S. Cooper
ASAlexandra Sinclair
Alexandra Sinclair
PSPaul M. Stewart
Paul M. Stewart
11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) interconverts the inactive glucocorticoid cortisone and its active form cortisol. It is widely expressed and, although bidirectional, in vivo it functions predominantly as an oxoreductase, generating active glucocorticoid. This allows glucocorticoid receptor activation to be regulated at a prereceptor level in a tissue-specific manner. In this review, we will discuss the enzymology and molecular biology of 11β-HSD1 and the molecular basis of cortisone reductase deficiencies. We will also address how altered 11β-HSD1 activity has been implicated in a number of disease states, and we will explore its role in the physiology and pathologies of different tissues. Finally, we will address the current status of selective 11β-HSD1 inhibitors that are in development and being tested in phase II trials for patients with the metabolic syndrome. Although the data are preliminary, therapeutic inhibition of 11β-HSD1 is also an exciting prospect for the treatment of a variety of other disorders such as osteoporosis, glaucoma, intracranial hypertension, and cognitive decline.