Peter J Goadsby

King's College London, Londinium, England, United Kingdom

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Publications (645)3599.73 Total impact

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    ABSTRACT: Hemicrania continua (HC) is a rare chronic headache disorder, typically accompanied by cranial autonomic features and responding to therapeutic doses of indomethacin. The pathophysiology of hemicrania continua is not fully understood. We report a series of three patients who developed a continuous hemicranial headache after cranial surgery. Each case presented a similar phenotype of continuous half-sided headache, cranial autonomic symptoms with exacerbations (2/3), and a response to indomethacin. The biology of hemicrania continua may be activated post-craniotomy just as can be seen with other primary headache disorders.
    The Journal of Headache and Pain 12/2015; 16(1):526. DOI:10.1186/s10194-015-0526-4 · 3.28 Impact Factor
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    ABSTRACT: Single pulse transcranial magnetic stimulation (sTMS) is a novel treatment for acute migraine. Previous randomised controlled data demonstrated that sTMS is effective and well tolerated in the treatment of migraine with aura. The aim of the programme reported here was to evaluate patient responses in the setting of routine clinical practice. Migraine patients with and without aura treating with sTMS had an initial review (n = 426) and training call, and then participated in telephone surveys at week six (n = 331) and week 12 during a 3-month treatment period (n = 190). Of patients surveyed with 3 month data (n = 190; episodic, n = 59; chronic, n = 131), 62 % reported pain relief, finding the device effective at reducing or alleviating migraine pain; in addition there was relief reported of associated features: nausea- 52 %; photophobia- 55 %; and phonophobia- 53 %. At 3 months there was a reduction in monthly headache days for episodic migraine, from 12 (median, 8-13 IQ range) to 9 (4-12) and for chronic migraine, a reduction from 24 (median, 16-30 IQ range) to 16 (10-30). There were no serious or unanticipated adverse events. sTMS may be a valuable addition to options for the treatment of both episodic and chronic migraine.
    The Journal of Headache and Pain 12/2015; 16(1):535. DOI:10.1186/s10194-015-0535-3 · 3.28 Impact Factor
  • Christoph J Schankin, Peter J Goadsby
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    ABSTRACT: Patients with visual snow complain of uncountable flickering tiny dots in the entire visual field similar to the view of a badly tuned analogue TV channel (TV snow). The symptoms are often continuous and can persist over years. This condition is grouped among the persistent visual phenomena in migraine, although it clinically presents a unique entity distinct from persistent migraine aura or migraine aura status. Here, we review the recent literature leading to the identification of the visual snow syndrome. The additional visual and non-visual symptoms are described in detail, and criteria are presented for future studies. Using these criteria, the relationship to migraine and typical migraine aura was recently evaluated. Further, patients with visual snow differ from controls in respect of hypermetabolism in the supplementary visual cortex (lingual gyrus). This provides evidence that visual snow, despite being purely subjective in the individual patient, has a clear biological basis. The area of hypermetabolism overlaps with the functional correlates of photophobia in migraine supporting the close relationship of migraine and visual snow.
    Current Pain and Headache Reports 06/2015; 19(6):497. DOI:10.1007/s11916-015-0497-9 · 2.26 Impact Factor
  • Amy R Tso, Peter J Goadsby
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    ABSTRACT: Neuroimaging techniques can be used to investigate both functional and structural features of the brain in patients who have primary headache disorders such as migraine or cluster headache. Improved treatments are needed for both, and this goal will likely be facilitated by a better understanding of the underlying biology. Functional imaging studies have identified regions active during attacks, as well as abnormalities that are present during the interictal period. Volumetric, surface-based morphometric, and tractography studies have revealed structural changes, although whether these represent a cause or effect of the condition remains to be determined. The development of new techniques and modalities promises to yield additional insights in the future. This article aims to review the major findings and most recent advances in neuroimaging of migraine and cluster headache.
    Current Pain and Headache Reports 06/2015; 19(6):487. DOI:10.1007/s11916-015-0487-y · 2.26 Impact Factor
  • Peter J Goadsby
    Neurology 05/2015; 84(21). DOI:10.1212/WNL.0000000000001623 · 8.30 Impact Factor
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    ABSTRACT: Background: Addressing the overuse of acute medicines is a challenging but crucial component of migraine treatment in clinical practice. sTMS has previously shown efficacy in reducing migraine symptoms and acute medicines in the UK pilot programme. Aim: To explore the utility of sTMS to treat migraine with acute medication overuse. Method: Patients (n¼28) were selected by their Neurologist in open clinical practice and advised to reduce their intake of acute medicines. Headache nurses provided treatment instructions and collected baseline and outcome data through telephone surveys at Baseline, 6- and 12- week time points. The patients were instructed to treat with sTMS twice daily and acutely at attack onset, using the sTMS Medical Advisory Board (TMS-MAB) guidelines. Patients were encouraged to reduce acute medicines during the treatment period; a rate of reduction was not stipulated. Results: Twenty-eight patients were prescribed sTMS and treated for 12 weeks. Of these: 86% (n¼24) reported a reduction in the number of days of acute medicine use, with 75% (n¼21) reporting reduced pain severity. Nineteen patients (68%) reported reduced migraine days and 15 (54%) had shorter attack duration. In addition, headache disability scores (HIT-6) were improved in 75% of patients (n¼21). The treatment was well tolerated and no adverse events were reported. Conclusion: sTMS may be an effective bridge treatment for patients with medication overuse. The majority of patients reduced acute treatments and reported efficacy for migraine symptoms.
  • Nazia Karsan, Peter J Goadsby
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    ABSTRACT: Migraine is a complex disorder of the brain that is common and highly disabling. As understanding of the neural pathways has advanced, and it has become clear that the vascular hypothesis does not explain the disorder, new therapeutic avenues have arisen. One such target is calcitonin gene-related peptide (CGRP)-based mechanisms. CGRP is found within the trigeminovascular nociceptive system widely from the trigeminal ganglion to second-order and third-order neurons and in regulatory areas in the brainstem. Studies have shown CGRP is released during severe migraine attacks and the reversal of the attack with effective triptan treatment normalizes those levels. CGRP administration triggers migraine in patients, and CGRP receptor antagonists have been shown to abort migraine. Here, we review the current state of CGRP mechanism antagonist therapy as its research and development is increasing in migraine therapeutics. We discuss several recent trials, highlighting the evidence base behind these novel drugs, and their potential future contribution to migraine management.
    Current Neurology and Neuroscience Reports 05/2015; 15(5):547. DOI:10.1007/s11910-015-0547-z · 3.67 Impact Factor
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    ABSTRACT: This review aims to understand the prevalence of premonitory symptoms in migraine, postulate their mechanisms, and compare these with functional imaging studies. A thorough literature review was conducted using PubMed for prevalence studies of premonitory symptoms in migraine and functional imaging studies in the premonitory phase. The majority of studies have been retrospective reporting a prevalence of 7-88% for premonitory symptoms in migraine. Only one study has investigated premonitory symptoms prospectively and used preselected patients with recognized premonitory symptoms. The majority of patients were able to predict correctly the onset of migraine headache. Only one functional imaging study has been conducted in the premonitory phase that showed activation of posterolateral hypothalamus, midbrain tegmental area and substantia nigra, periaqueductal gray, dorsal pons, and various cortical areas including occipital, temporal, and prefrontal cortex. Subgroup analysis of patients with photophobia more than without photophobia in the premonitory phase showed activation of the occipital cortex. Comparison of patients with nausea more than without nausea in the premonitory phase showed activation in upper dorsal medulla and periaqueductal gray. Premonitory symptoms are common in migraine, although the true prevalence cannot be stated with certainty in the absence of prospective studies in unselected patients. Hypothalamic involvement can explain many of the premonitory symptoms. Activation of the the brainstem structures and hypothalamus before pain suggests a pivotal role of these structures in the pathogenesis of migraine. Hypersensitivity to light and occurrence of nausea in migraine is associated with activation of central brain structures involved in these pathways, and this can occur in the absence of pain. © 2015 American Headache Society.
    Headache The Journal of Head and Face Pain 04/2015; 55(5). DOI:10.1111/head.12572 · 3.19 Impact Factor
  • Nazia Karsan, Peter J Goadsby
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    ABSTRACT: Migraine is a common, complex disorder of the brain with significant morbidity. As the pathophysiology of the disorder has become better appreciated, the role of neuropeptides has been explored. Calcitonin gene-related peptide (CGRP) has emerged as a promising therapeutic target. CGRP is widely distributed in the nervous system, particularly at anatomical areas thought to be involved with migraine, including the trigeminovascular nociceptive system. In studies, CGRP has been shown to be released during severe migraine attacks, and effective triptan treatment of an attack normalizes these levels. CGRP administration triggers migraine in patients and CGRP receptor antagonists can abort migraine. Moreover, recent data demonstrate that CGRP mechanism blockade either by small molecule receptor antagonists or by monoclonal antibodies can have a preventive effect in migraine. This article highlights the evidence behind the role of CGRP in migraine and the state of CGRP-based mechanism treatment development. We present a summary of the evidence base behind CGRP in migraine pathophysiology and the novel CGRP mechanism drugs and their potential future contribution to migraine management in our clinical practice.
    Current opinion in neurology 04/2015; 28(3). DOI:10.1097/WCO.0000000000000191 · 5.73 Impact Factor
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    ABSTRACT: To determine whether acute migraine treatment outcome is different in migraine with aura compared with migraine without aura. We examined pooled outcome data for sumatriptan treatment of migraine with and without aura from the sumatriptan/naratriptan aggregate patient database. We also examined similar outcome data for inhaled dihydroergotamine (DHE) from a single, large randomized controlled study. The pooled pain-free rates 2 hours postdose for sumatriptan 100 mg were significantly higher in patients treating attacks without aura (32%) compared with the group who treated attacks with aura (24%) (p < 0.001). The relative risk for pain freedom 2 hours postdose for attacks without aura was 1.33 (95% confidence interval: 1.16-1.54). The number needed to treat for 2 hours of pain freedom was 4.4 for attacks without aura and 6.2 for attacks with aura. For the clinical trial of DHE, the 2-hour pain-free rates did not differ between patients treating attacks without aura (29.4%) compared with those who treated attacks with aura (27.2%; p = 0.65). The relative risk for pain freedom 2 hours postdose for attacks without aura vs with aura was 1.08 (95% confidence interval: 0.77-1.53). The number needed to treat for 2 hours pain free was 5.8 for attacks without aura and 5.0 for attacks with aura. This post hoc analysis of pooled data from multiple randomized trials indicates that sumatriptan is less effective as acute therapy for migraine attacks with aura compared with attacks without aura. In the single study of inhaled DHE, the treatment had similar efficacy for migraine attacks with and without aura. Different responses of migraine with vs without aura to acute therapies may provide insight into underlying migraine mechanisms and influence the choice of acute therapies for different types of migraine attacks. © 2015 American Academy of Neurology.
    Neurology 04/2015; 84(18). DOI:10.1212/WNL.0000000000001535 · 8.30 Impact Factor
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    ABSTRACT: Calcitonin gene-related peptide (CGRP) receptor antagonism is an approach to migraine therapy. The locus of action of antimigraine treatment is not resolved. The objective was to investigate CGRP receptors in the ventrolateral periaqueductal gray (vlPAG) involved in the modulation of trigeminovascular nociception by descending influences on neurotransmission. The presence of calcitonin receptor-like receptor (CLR) and receptor activity modifying protein 1 (RAMP1), which form functional CGRP receptors, was investigated. CGRP and its receptor antagonists, olcegepant and CGRP (8-37), were microinjected into the vlPAG while changes of neural responses in the trigeminocervical complex (TCC) were monitored. Immunoreactivity indicated the presence of functional CGRP receptor components in the vlPAG and adjacent mesencephalic trigeminal nucleus. Inhibition of TCC responses to stimulation of dural afferents and ophthalmic cutaneous receptive fields after microinjection of bicuculline into vlPAG indicated a connection between the vlPAG and TCC neurons. CGRP facilitated these TCC responses, whereas olcegepant and CGRP (8-37) decreased them. CGRP and its receptor antagonists act on neurons in the region of vlPAG to influence nociceptive transmission in the TCC. This suggests CGRP receptor antagonists may act at loci outside of the TCC and reinforces the concept of migraine as a disorder of the brain. © International Headache Society 2015 Reprints and permissions:
    Cephalalgia 03/2015; DOI:10.1177/0333102415576723 · 4.12 Impact Factor
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    ABSTRACT: Our understanding of risk factors for childhood stroke is incomplete. In adults, migraine with aura is associated with a two-fold increase in ischemic stroke risk. In this cohort study we examine the association between migraine and stroke among children in Kaiser Permanente Northern California (KPNC). Children ages 2-17 years who were members of KPNC for ≥6 months between 1997 and 2007 were included. Migraine cohort members had one or more of: an ICD-9 code for migraine, migraine listed as a significant health problem, or a prescription for a migraine-specific medication. The comparison group was children with no evidence of headache. Main outcome measures included stroke incidence rates and incidence rate ratios (IR). Among the 1,566,952 children within KPNC during the study period, 88,164 had migraine, and 1,323,142 had no evidence of headache. Eight migraineurs had a stroke (three (38%) hemorrhagic; five (63%) ischemic). Eighty strokes occurred in children without headache (53 (66%) hemorrhagic; 27 (34%) ischemic). The ischemic stroke incidence rate was 0.9/100,000 person-years in migraineurs vs. 0.4/100,000 person-years in those without headache; IR 2.0 (95% CI 0.8-5.2). A post-hoc analysis of adolescents (12-17 years) showed an increased risk of ischemic stroke among those with migraine; IR 3.4 (95% CI 1.2-9.5). The hemorrhagic stroke incidence rate was 0.5/100,000 person-years in migraineurs and 0.9/100,000 person-years in those without headache; IR 0.6 (95% CI 0.2-2.0). There was no statistically significant increase in hemorrhagic or ischemic stroke risk in pediatric migraineurs in this cohort study. A post-hoc analysis found that ischemic stroke risk was significantly elevated in adolescents with migraine. Future studies should focus on identifying risk factors for ischemic stroke among adolescent migraineurs. Based on adult data, we recommend that migraine aura status should be studied as a possible risk factor for ischemic stroke among adolescent migraineurs. © International Headache Society 2015 Reprints and permissions:
    Cephalalgia 03/2015; DOI:10.1177/0333102415576222 · 4.12 Impact Factor
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    ABSTRACT: Migraine is a common and disabling neurologic disorder, with important psychiatric comorbidities. Its pathophysiology involves activation of neurons in the trigeminocervical complex (TCC). Kainate receptors carrying the glutamate receptor subunit 5 (GluK1) are present in key brain areas involved in migraine pathophysiology. To study the influence of kainate receptors on trigeminovascular neurotransmission, we determined the presence of GluK1 receptors within the trigeminal ganglion and TCC with immunohistochemistry. We performed in vivo electrophysiologic recordings from TCC neurons and investigated whether local or systemic application of GluK1 receptor antagonists modulated trigeminovascular transmission. Microiontophoretic application of a selective GluK1 receptor antagonist, but not of a nonspecific ionotropic glutamate receptor antagonist, markedly attenuated cell firing in a subpopulation of neurons activated in response to dural stimulation, consistent with selective inhibition of postsynaptic GluK1 receptor-evoked firing seen in all recorded neurons. In contrast, trigeminovascular activation was significantly facilitated in a different neuronal population. The clinically active kainate receptor antagonist LY466195 attenuated trigeminovascular activation in all neurons. In addition, LY466195 demonstrated an N-methyl-d-aspartate receptor-mediated effect. This study demonstrates a differential role of GluK1 receptors in the TCC, antagonism of which can inhibit trigeminovascular activation through postsynaptic mechanisms. Furthermore, the data suggest a novel, possibly presynaptic, modulatory role of trigeminocervical kainate receptors in vivo. Differential activation of kainate receptors suggests unique roles for this receptor in pro- and antinociceptive mechanisms in migraine pathophysiology.
    Pain 03/2015; 156(3):439-450. DOI:10.1097/01.j.pain.0000460325.25762.c0 · 5.84 Impact Factor
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    ABSTRACT: To report our initial experience with a novel device, designed to provide portable, noninvasive, transcutaneous stimulation of the vagus nerve, both acutely and preventively, as a treatment for cluster headache. Patients with cluster headache (11 chronic, 8 episodic), from 2 centers, including 7 who were refractory to drug treatment, had sufficient data available for analysis in this open-label observational cohort study. The device, known as the gammaCore, was used acutely to treat individual attacks as well as to provide prevention. Patient-estimated efficacy data were collected by systematic inquiry during follow-up appointments up to a period of 52 weeks of continuous use. Fifteen patients reported an overall improvement in their condition, with 4 reporting no change, providing a mean overall estimated improvement of 48%. Of all attacks treated, 47% were aborted within an average of 11 ± 1 minutes of commencing stimulation. Ten patients reduced their acute use of high-flow oxygen by 55% with 9 reducing triptan use by 48%. Prophylactic use of the device resulted in a substantial reduction in estimated mean attack frequency from 4.5/24 hours to 2.6/24 hours (p < 0.0005) posttreatment. These data suggest that noninvasive vagus nerve stimulation may be practical and effective as an acute and preventive treatment in chronic cluster headache. Further evaluation of this treatment using randomized sham-controlled trials is thus warranted. This study provides Class IV evidence that for patients with cluster headache, transcutaneous stimulation of the vagus nerve aborts acute attacks and reduces the frequency of attacks. © 2015 American Academy of Neurology.
    Neurology 02/2015; 84(12). DOI:10.1212/WNL.0000000000001394 · 8.30 Impact Factor
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    ABSTRACT: We sought to explore whether patients with migraine show heightened interictal intrinsic connectivity within primary sensory networks, the salience network, and a network anchored by the dorsal pons, a region known to be active during migraine attacks. Using task-free fMRI and a region-of-interest analysis, we compared intrinsic connectivity patterns in 15 migraineurs without aura to 15 age- and sex-matched healthy controls, focusing on networks anchored by the calcarine cortex, Heschl gyrus, right anterior insula, and dorsal pons, a region active during migraine attacks. We also examined the relationship between network connectivity, migraine frequency, and sensory sensitivity symptoms. Migraineurs showed increased connectivity between primary visual and auditory cortices and the right dorsal anterior insula, between the dorsal pons and the bilateral anterior insulae, and between the right and left ventral anterior insulae. Increased connectivity showed no clinical correlation with migraine frequency or sensory sensitivity. Patients with migraine display interictal changes in the topology of intrinsic connections, with greater connectivity between primary sensory cortices, the pons, and the anterior insula, a region involved in representing and coordinating responses to emotional salience. © 2015 American Academy of Neurology.
    Neurology 02/2015; 84(10). DOI:10.1212/WNL.0000000000001330 · 8.30 Impact Factor
  • Peter J Goadsby
    Cephalalgia 01/2015; 35(5). DOI:10.1177/0333102414566196 · 4.12 Impact Factor
  • The Lancet Neurology 01/2015; 14(1):32-3. DOI:10.1016/S1474-4422(14)70309-6 · 21.82 Impact Factor
  • Simon Akerman, Peter J Goadsby
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    ABSTRACT: Trigeminal autonomic cephalalgias (TACs) are highly disabling primary headache disorders that involve severe unilateral head pain coupled with significant lateralized cranial autonomic features. Our understanding of these disorders and the development of novel and more effective treatments has been limited by the lack of a suitable animal model to explore their pathophysiology and screen prospective treatments. This review details the development of a novel preclinical model that demonstrates activation of both the trigeminovascular system and parasympathetic projections, thought to be responsible for the severe head pain and autonomic symptoms. This model demonstrates a unique response to TAC specific treatments and highlights the importance of the cranial parasympathetic pathway to the pathophysiology of TACs and as a potential locus of action for treatments. The development of this model opens up opportunities to understand the pathophysiology of these disorders further, the likely involvement of the hypothalamus, as well as providing a preclinical model with which to screen novel compounds. © 2015 American Headache Society.
    Headache The Journal of Head and Face Pain 01/2015; 55(1):197-203. DOI:10.1111/head.12471 · 3.19 Impact Factor
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    ABSTRACT: Background We have argued against the traditional approach of counselling avoidance of all triggers of headaches and migraine. Problems with this approach include the impossibility of avoiding all triggers and the high costs associated with trying to do so, and that avoidance could lead to reduced tolerance for the triggers. We have developed an alternative approach called Learning to Cope with Triggers (LCT) that encourages avoidance of triggers that are detrimental to health and wellbeing, but uses exposure to other triggers to desensitise headache sufferers to the triggers. This approach has been shown to be more effective than advising avoidance of all triggers. Trigger management is only one component of a comprehensive treatment program and the current study is designed to evaluate a new approach to treating headaches in which LCT has been integrated into an established cognitive-behavioural therapy (CBT) package (LCT/CBT).Methods/DesignA target sample of 120 adult participants who suffer from migraine or tension-type headache, at least six days per month, and have done so for at least 12 months will be recruited. Participants will be randomly assigned to one of three groups: LCT/CBT; Avoid/CBT (CBT combined with instructions to avoid all triggers); and waiting-list control. Measures will include: daily diaries for recording headaches, triggers and medication consumption; headache disability and quality of life; trigger avoidance; locus of control and self-efficacy; and coping strategies. Treatment will involve 12 60-minute sessions scheduled weekly. Assessment will be completed before and after treatment, and at 4 and 12 month follow-up. The data will be analysed to determine which approach is most effective, and predictors of response to treatment.DiscussionMigraine and tension-type headache are common and can be disabling. CBT has been demonstrated to be an efficacious treatment for both disorders. However, there is room for improvement. This study aims to increase the efficacy of behavioural approaches and identify factors predictive of a positive response.Trial registrationAustralian and New Zealand Clinical Trials Registry ACTRN12614000435684.
    BMC Neurology 12/2014; 14(1):233. DOI:10.1186/s12883-014-0233-9 · 2.49 Impact Factor
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    ABSTRACT: Nausea is a common and disabling symptom of migraine. The origin of nausea is not well understood although functional connections between trigeminal neurons and the nucleus tractus solitarius may explain occurrence of nausea with pain. However, nausea occurs as a premonitory symptom in about a quarter of patients, suggesting that a primary brain alteration unrelated to the experience of pain may be the reason for nausea. We performed positron emission tomography scans with H215O PET in premonitory phase of nitroglycerin-induced migraine and compared patients with and without nausea. The results showed activation in rostral dorsal medulla and periaqueductal grey (PAG) in the nausea group, which was absent in the no nausea group. The rostral dorsal medullary area included the nucleus tractus solitarius, dorsal motor nucleus of the vagus nerve and the nucleus ambiguus, all of which are thought to be involved in brain circuits mediating nausea. The results demonstrate that nausea can occur as a premonitory symptom in migraine, independent of pain and trigeminal activation. This is associated with activation of brain structures known to be involved in nausea. We conclude that nausea is a centrally driven symptom in migraine.
    The Journal of Headache and Pain 12/2014; 15(1):84. DOI:10.1186/1129-2377-15-84 · 3.28 Impact Factor

Publication Stats

27k Citations
3,599.73 Total Impact Points


  • 2014–2015
    • King's College London
      Londinium, England, United Kingdom
    • ICL
      Londinium, England, United Kingdom
  • 2007–2015
    • University of California, San Francisco
      • Department of Neurology
      San Francisco, California, United States
  • 2013
    • University of California, Los Angeles
      Los Ángeles, California, United States
    • Stanford University
      • Stanford Prevention Research Center
      Palo Alto, California, United States
  • 2012
    • University of Surrey
      • Surrey Sleep Research Centre (SSRC)
      Guildford, ENG, United Kingdom
  • 2011
    • University of Alberta
      • Division of Neurology
      Edmonton, Alberta, Canada
    • San Francisco VA Medical Center
      San Francisco, California, United States
  • 2009–2011
    • University Medical Center Schleswig-Holstein
      Kiel, Schleswig-Holstein, Germany
    • UCL Eastman Dental Institute
      Londinium, England, United Kingdom
  • 1986–2011
    • Prince Henry's Institute
      Melbourne, Victoria, Australia
  • 2010
    • University of Iowa
      Iowa City, Iowa, United States
    • Washington University in St. Louis
      San Luis, Missouri, United States
  • 2009–2010
    • CSU Mentor
      • Department of Neurology
      Long Beach, California, United States
  • 2003–2009
    • Glostrup Hospital
      • Department of Neurology
      København, Capital Region, Denmark
    • University of Münster
      • Department of Neurology
      Münster, North Rhine-Westphalia, Germany
  • 2008
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
    • University of Bristol
      • School of Social and Community Medicine
      Bristol, England, United Kingdom
    • University of Duisburg-Essen
      • Erwin L. Hahn Institute for Magnetic Resonance Imaging
      Essen, North Rhine-Westphalia, Germany
  • 2006–2008
    • Ghent University
      • Neurology
      Gent, VLG, Belgium
    • University of Hamburg
      Hamburg, Hamburg, Germany
  • 2001–2008
    • University College London
      • Institute of Neurology
      Londinium, England, United Kingdom
  • 2001–2007
    • Albert Einstein College of Medicine
      • Department of Neuroradiology
      New York, New York, United States
  • 1997–2007
    • London Research Institute
      Londinium, England, United Kingdom
  • 2002–2005
    • Leiden University Medical Centre
      • Department of Neurology
      Leiden, South Holland, Netherlands
    • Kansas City VA Medical Center
      Kansas City, Missouri, United States
  • 2001–2005
    • Indian Broiler (IB) Group India
      Bhānpuri, Chhattisgarh, India
  • 1999–2005
    • Thomas Jefferson University
      • Department of Neurology
      Philadelphia, Pennsylvania, United States
  • 2004
    • WWF United Kingdom
      Londinium, England, United Kingdom
    • Mayo Clinic - Scottsdale
      Scottsdale, Arizona, United States
  • 2000–2002
    • Thomas Jefferson University Hospitals
      • Department of Neurology
      Philadelphia, Pennsylvania, United States
    • Keele University
      Newcastle-under-Lyme, England, United Kingdom
  • 1998
    • University of London
      Londinium, England, United Kingdom
    • Gold Coast University Hospital
      Southport, Queensland, Australia
  • 1990–1996
    • Lund University
      Lund, Skåne, Sweden
  • 1983–1994
    • University of New South Wales
      • • Institute of Neurological Sciences
      • • Department of Medicine
      Kensington, New South Wales, Australia
  • 1991
    • University of South Wales
      Понтиприте, Wales, United Kingdom
  • 1990–1991
    • Prince of Wales Hospital and Community Health Services
      • • Institute of Neurological Sciences
      • • Department of Neurology
      Sydney, New South Wales, Australia