Head TraumaPhase 2KETABRAINNCT02232347
Ketamine and Glutamate After Brain Injury : a Microdialysis Study
A Phase 2 study testing Ketamine and Sufentanil in people with Head Trauma, run by Pierre-Julien CUNGI at 1 site in France.
Trial summary
The objective of the study is to compare the effects of 48 hours ketamine infusion versus sufentanil infusion on brain glutamate concentrations measured with microdialysis after traumatic brain injury. We hypothesize that ketamine infusion will decrease high glutamate values faster than sufentanil. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Head Trauma
- What is being tested?
- Ketamine and Sufentanil
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 20 participants
- Where
- 1 siteFrance
- Study dates
- Oct 2014to May 2017
- Phase
- Phase 2
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- > 18 years old
- Glasgow Coma Scale (GCS) < 9
- > 3 days of sedation expected at the arrival
Who cannot join
- pregnancy
- < 18 years old
- estimated survival < 48 hours post-trauma
- expected sedation < 3 days
- coagulation impairment (platelets<100.000/mm3 and prothrombin time (TP) <60%)
- Cardiac arrest before ICU admission
Show all 10Show fewer
- Admission > 12 hours after trauma
- Multimodal monitoring implanted > 24 hours post trauma
- Participation to the study refused by the next of kind
- No next of kind
Trial locations and contacts
1 site in 1 country.
France1 site
Sainte Anne Military Teaching Hospital
Toulon, 83130
Pierre Julien CUNGI, MD
Eric MEAUDRE, MD
About this study
Official title: Effect of Ketamine Versus Sufentanil on Cerebral Glutamate After Traumatic Brain Injury : a Randomized, Double-blinded, Microdialysis Study
The objective of the study is to compare the effects of 48 hours ketamine infusion versus sufentanil infusion on brain glutamate concentrations measured with microdialysis after traumatic brain injury.
We hypothesize that ketamine infusion will decrease high glutamate values faster than sufentanil.
Read the detailed description
Inclusion of 20 consecutive head trauma patients. Randomization and double-blind to compare the effects of ketamine versus sufentanil on brain glutamate concentrations measured with microdialysis.
Ketamine is an anti-N-methyl-D-aspartate (NMDA) medication. It is supposed to limit excitotoxicity of amino-acids, especially glutamate. Glutamate is known to be elevated in more than 60% of the severe head trauma patients. It induces cortical spreading depression which can aggravate prognosis. It's a daily used medication in anesthesia and intensive care units for sedation and induction of anesthesia. It's the recommended medication for induction of unstable wounded soldiers on the field because of its neutrality on haemodynamic state.
Sufentanil is the reference opioid for sedation in ICU in Europe. It can induce hypotension which is deleterious for cerebral perfusion pressure after brain trauma.
In our unit, patients with severe head injury are monitored by a triple lumen access device including ICP (IntraCerebral Pressure), PtiO2 (oxygen pressure in the brain) and microdialysis. This last monitoring allows measurement of brain parenchymal concentrations of small molecules : glucose, lactate, pyruvate, glutamate, glycerol,.... It's a tool to evaluate the metabolic state of the brain divided into 4 categories : normal, hyperglycolysis, ischemia and metabolic crisis.
Then, we will detail the effects of ketamine on metabolic state of the brain, especially glutamate concentration. Normal values are below 10 micromol/ml. After head trauma it can dramatically increase to values up to 50 or even 100 micromol/ml, with normalization after 24 hours. Ketamine is expected to decrease these high values faster than described in observational studies.
- Conditions
- Head Trauma
- Being tested
- Ketamine, Sufentanil
- Keywords
- traumatic brain injury, ketamine, microdialysis, PtiO2, glutamate
- Medical subject headings
- Craniocerebral Trauma, Brain Injuries, Traumatic
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
KetamineDrug
SufentanilDrug
| Study group | Role | What they receive |
|---|---|---|
| ketamine | Experimental | ketamine 5 mg/kg/h, continuous infusion for 48 hours Receives: Drug: Ketamine |
| sufentanil | Active comparator | sufentanil 0,5 mcg/kg/h, continuous infusion for 48 hours Receives: Drug: Sufentanil |
What is being measured
The primary outcome is the main question the study is designed to answer.
brain glutamate concentrations
To compare the kinetic of brain glutamate concentration decrease during 4 periods of 12 hours between ketamine infusion group (KET) and sufentanil standard infusion group (STD)
Measured: H0-H12, H12-H24, H24-H36 and H36-H48
Secondary outcomes (4)
metabolic profile
To compare the brain metabolic profile (normal, ischemic, hyperglycolytic and metabolic crisis) of the patients related to their group of treatment : ketamine (KET) and sufentanil (STD) by measuring brain glucose, brain lactate, brain glycerol concentrations and brain lactate/pyruvate ratio.
Measured: H0-H12, H12-H24, H24-H36 and H36-H48
Episodes of intracranial hypertension (ICHT) and brain ischemia
To compare the number of ICHT episodes (ICP>20 mm Hg more than 15 minutes) and to compare the number of ischemic episodes (PtiO2<20 mm Hg more than 15 minutes) between the 2 groups
Measured: H0-H12, H12-H24, H24-H36 and H36-H48
Therapeutic Intensity Level (TIL)
To compare the TIL value between the 2 groups. TIL is a score developed to measure the intensity of cares for head trauma patients. Lower scores are meaning less intense cares. It is calculated for 24 hours periods.
Measured: Days 1 and 2
Glasgow Outcome Scale (GOS) et extended Glasgow Outcome Scale (eGOS)
To describe the prognosis of the patients of the KETAMINE group versus SUFENTANIL group. GOS is the international validated score for evaluation of the prognosis after head trauma.
Measured: 6 months and 1 year
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Sep 2014 (estimated)
- Study startOct 2014
- Primary completionOct 2016 (estimated)
- Study completionMay 2017 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for Head TraumaStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 20 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Pierre-Julien CUNGI
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor-investigator, Pierre-Julien CUNGI, Direction Centrale du Service de Santé des Armées
- Investigators
- Ambroise MONTCRIOL, MD, Principal investigator, Direction Centrale du Service de Santé des Armées
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02232347
- Sponsor's protocol ID
- DCSSA KETABRAIN
- Acronym
- KETABRAIN
- Status last verified
- Sep 2014
- First submitted
- 2 Sep 2014
- Last updated
- 5 Sep 2014
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS; Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13. doi: 10.1089/neu.2007.9995. No abstract available.
PubMed 17511549Hughes S. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: is ketamine a viable induction agent for the trauma patient with potential brain injury. Emerg Med J. 2011 Dec;28(12):1076-7. doi: 10.1136/emermed-2011-200891.
PubMed 22101599Filanovsky Y, Miller P, Kao J. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. CJEM. 2010 Mar;12(2):154-7. doi: 10.1017/s1481803500012197. No abstract available.
PubMed 20219164Hudetz JA, Pagel PS. Neuroprotection by ketamine: a review of the experimental and clinical evidence. J Cardiothorac Vasc Anesth. 2010 Feb;24(1):131-42. doi: 10.1053/j.jvca.2009.05.008. Epub 2009 Jul 29. No abstract available.
PubMed 19640746Ward JL, Harting MT, Cox CS Jr, Mercer DW. Effects of ketamine on endotoxin and traumatic brain injury induced cytokine production in the rat. J Trauma. 2011 Jun;70(6):1471-9. doi: 10.1097/TA.0b013e31821c38bd.
PubMed 21817985Bhutta AT, Schmitz ML, Swearingen C, James LP, Wardbegnoche WL, Lindquist DM, Glasier CM, Tuzcu V, Prodhan P, Dyamenahalli U, Imamura M, Jaquiss RD, Anand KJ. Ketamine as a neuroprotective and anti-inflammatory agent in children undergoing surgery on cardiopulmonary bypass: a pilot randomized, double-blind, placebo-controlled trial. Pediatr Crit Care Med. 2012 May;13(3):328-37. doi: 10.1097/PCC.0b013e31822f18f9.
PubMed 21926656Sakowitz OW, Kiening KL, Krajewski KL, Sarrafzadeh AS, Fabricius M, Strong AJ, Unterberg AW, Dreier JP. Preliminary evidence that ketamine inhibits spreading depolarizations in acute human brain injury. Stroke. 2009 Aug;40(8):e519-22. doi: 10.1161/STROKEAHA.109.549303. Epub 2009 Jun 11.
PubMed 19520992Hartings JA, Bullock MR, Okonkwo DO, Murray LS, Murray GD, Fabricius M, Maas AI, Woitzik J, Sakowitz O, Mathern B, Roozenbeek B, Lingsma H, Dreier JP, Puccio AM, Shutter LA, Pahl C, Strong AJ; Co-Operative Study on Brain Injury Depolarisations. Spreading depolarisations and outcome after traumatic brain injury: a prospective observational study. Lancet Neurol. 2011 Dec;10(12):1058-64. doi: 10.1016/S1474-4422(11)70243-5. Epub 2011 Nov 3.
PubMed 22056157Raboel PH, Bartek J Jr, Andresen M, Bellander BM, Romner B. Intracranial Pressure Monitoring: Invasive versus Non-Invasive Methods-A Review. Crit Care Res Pract. 2012;2012:950393. doi: 10.1155/2012/950393. Epub 2012 Jun 8.
PubMed 22720148Stuart RM, Schmidt M, Kurtz P, Waziri A, Helbok R, Mayer SA, Lee K, Badjatia N, Hirsch LJ, Connolly ES, Claassen J. Intracranial multimodal monitoring for acute brain injury: a single institution review of current practices. Neurocrit Care. 2010 Apr;12(2):188-98. doi: 10.1007/s12028-010-9330-9.
PubMed 20107926Bourgoin A, Albanese J, Wereszczynski N, Charbit M, Vialet R, Martin C. Safety of sedation with ketamine in severe head injury patients: comparison with sufentanil. Crit Care Med. 2003 Mar;31(3):711-7. doi: 10.1097/01.CCM.0000044505.24727.16.
PubMed 12626974Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viviand X, Martin C. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severely brain-injured patients. Crit Care Med. 2005 May;33(5):1109-13. doi: 10.1097/01.ccm.0000162491.26292.98.
PubMed 15891344Chamoun R, Suki D, Gopinath SP, Goodman JC, Robertson C. Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury. J Neurosurg. 2010 Sep;113(3):564-70. doi: 10.3171/2009.12.JNS09689.
PubMed 20113156
Study at a glance
From the registry record, last updated by the sponsor on 5 Sep 2014. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effect of Ketamine Versus Sufentanil on Cerebral Glutamate After Traumatic Brain Injury : a Randomized, Double-blinded, Microdialysis Study
- ClinicalTrials.gov ID
- NCT02232347
- Acronym / sponsor ID
- KETABRAIN / DCSSA KETABRAIN
- Conditions
- Head Trauma
- Keywords
- traumatic brain injury, ketamine, microdialysis, PtiO2, glutamate
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 20 participants (estimated)
- Lead sponsor
- Pierre-Julien CUNGIUniversity, hospital or other
- Study start
- Oct 2014
- Primary completion
- Oct 2016 (estimated)
- Study completion
- May 2017 (estimated)
- First posted
- 5 Sep 2014 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The objective of the study is to compare the effects of 48 hours ketamine infusion versus sufentanil infusion on brain glutamate concentrations measured with microdialysis after traumatic brain injury.
We hypothesize that ketamine infusion will decrease high glutamate values faster than sufentanil.
Detailed description
Inclusion of 20 consecutive head trauma patients. Randomization and double-blind to compare the effects of ketamine versus sufentanil on brain glutamate concentrations measured with microdialysis.
Ketamine is an anti-N-methyl-D-aspartate (NMDA) medication. It is supposed to limit excitotoxicity of amino-acids, especially glutamate. Glutamate is known to be elevated in more than 60% of the severe head trauma patients. It induces cortical spreading depression which can aggravate prognosis. It's a daily used medication in anesthesia and intensive care units for sedation and induction of anesthesia. It's the recommended medication for induction of unstable wounded soldiers on the field because of its neutrality on haemodynamic state.
Sufentanil is the reference opioid for sedation in ICU in Europe. It can induce hypotension which is deleterious for cerebral perfusion pressure after brain trauma.
In our unit, patients with severe head injury are monitored by a triple lumen access device including ICP (IntraCerebral Pressure), PtiO2 (oxygen pressure in the brain) and microdialysis. This last monitoring allows measurement of brain parenchymal concentrations of small molecules : glucose, lactate, pyruvate, glutamate, glycerol,.... It's a tool to evaluate the metabolic state of the brain divided into 4 categories : normal, hyperglycolysis, ischemia and metabolic crisis.
Then, we will detail the effects of ketamine on metabolic state of the brain, especially glutamate concentration. Normal values are below 10 micromol/ml. After head trauma it can dramatically increase to values up to 50 or even 100 micromol/ml, with normalization after 24 hours. Ketamine is expected to decrease these high values faster than described in observational studies.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| ketamine | Experimental | Drug: Ketamineketamine 5 mg/kg/h, continuous infusion for 48 hours |
| sufentanil | Active comparator | Drug: Sufentanilsufentanil 0,5 mcg/kg/h, continuous infusion for 48 hours |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- > 18 years old
- Glasgow Coma Scale (GCS) < 9
- > 3 days of sedation expected at the arrival
Key exclusion criteria (10 listed)
- pregnancy
- < 18 years old
- estimated survival < 48 hours post-trauma
- expected sedation < 3 days
- coagulation impairment (platelets<100.000/mm3 and prothrombin time (TP) <60%)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Ketamine | Drug | ketamine |
| Sufentanil | Drug | sufentanil |
Primary outcome
brain glutamate concentrations
Time frame: H0-H12, H12-H24, H24-H36 and H36-H48
To compare the kinetic of brain glutamate concentration decrease during 4 periods of 12 hours between ketamine infusion group (KET) and sufentanil standard infusion group (STD)
4 secondary outcomes
metabolic profile
Time frame: H0-H12, H12-H24, H24-H36 and H36-H48
Episodes of intracranial hypertension (ICHT) and brain ischemia
Time frame: H0-H12, H12-H24, H24-H36 and H36-H48
Therapeutic Intensity Level (TIL)
Time frame: Days 1 and 2
Glasgow Outcome Scale (GOS) et extended Glasgow Outcome Scale (eGOS)
Time frame: 6 months and 1 year
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 5 Sep 2014.
- Background: PubMed 17511549Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS; Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. Guidelines for the management of severe traumatic brain injury. I. Blood pressure and oxygenation. J Neurotrauma. 2007;24 Suppl 1:S7-13. doi: 10.1089/neu.2007.9995. No abstract available.
- Background: PubMed 22101599Hughes S. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 3: is ketamine a viable induction agent for the trauma patient with potential brain injury. Emerg Med J. 2011 Dec;28(12):1076-7. doi: 10.1136/emermed-2011-200891.
- Background: PubMed 20219164Filanovsky Y, Miller P, Kao J. Myth: Ketamine should not be used as an induction agent for intubation in patients with head injury. CJEM. 2010 Mar;12(2):154-7. doi: 10.1017/s1481803500012197. No abstract available.
- Background: PubMed 19640746Hudetz JA, Pagel PS. Neuroprotection by ketamine: a review of the experimental and clinical evidence. J Cardiothorac Vasc Anesth. 2010 Feb;24(1):131-42. doi: 10.1053/j.jvca.2009.05.008. Epub 2009 Jul 29. No abstract available.
- Background: PubMed 21817985Ward JL, Harting MT, Cox CS Jr, Mercer DW. Effects of ketamine on endotoxin and traumatic brain injury induced cytokine production in the rat. J Trauma. 2011 Jun;70(6):1471-9. doi: 10.1097/TA.0b013e31821c38bd.
- Background: PubMed 21926656Bhutta AT, Schmitz ML, Swearingen C, James LP, Wardbegnoche WL, Lindquist DM, Glasier CM, Tuzcu V, Prodhan P, Dyamenahalli U, Imamura M, Jaquiss RD, Anand KJ. Ketamine as a neuroprotective and anti-inflammatory agent in children undergoing surgery on cardiopulmonary bypass: a pilot randomized, double-blind, placebo-controlled trial. Pediatr Crit Care Med. 2012 May;13(3):328-37. doi: 10.1097/PCC.0b013e31822f18f9.
- Background: PubMed 19520992Sakowitz OW, Kiening KL, Krajewski KL, Sarrafzadeh AS, Fabricius M, Strong AJ, Unterberg AW, Dreier JP. Preliminary evidence that ketamine inhibits spreading depolarizations in acute human brain injury. Stroke. 2009 Aug;40(8):e519-22. doi: 10.1161/STROKEAHA.109.549303. Epub 2009 Jun 11.
- Background: PubMed 22056157Hartings JA, Bullock MR, Okonkwo DO, Murray LS, Murray GD, Fabricius M, Maas AI, Woitzik J, Sakowitz O, Mathern B, Roozenbeek B, Lingsma H, Dreier JP, Puccio AM, Shutter LA, Pahl C, Strong AJ; Co-Operative Study on Brain Injury Depolarisations. Spreading depolarisations and outcome after traumatic brain injury: a prospective observational study. Lancet Neurol. 2011 Dec;10(12):1058-64. doi: 10.1016/S1474-4422(11)70243-5. Epub 2011 Nov 3.
- Background: PubMed 22720148Raboel PH, Bartek J Jr, Andresen M, Bellander BM, Romner B. Intracranial Pressure Monitoring: Invasive versus Non-Invasive Methods-A Review. Crit Care Res Pract. 2012;2012:950393. doi: 10.1155/2012/950393. Epub 2012 Jun 8.
- Background: PubMed 20107926Stuart RM, Schmidt M, Kurtz P, Waziri A, Helbok R, Mayer SA, Lee K, Badjatia N, Hirsch LJ, Connolly ES, Claassen J. Intracranial multimodal monitoring for acute brain injury: a single institution review of current practices. Neurocrit Care. 2010 Apr;12(2):188-98. doi: 10.1007/s12028-010-9330-9.
- Background: PubMed 12626974Bourgoin A, Albanese J, Wereszczynski N, Charbit M, Vialet R, Martin C. Safety of sedation with ketamine in severe head injury patients: comparison with sufentanil. Crit Care Med. 2003 Mar;31(3):711-7. doi: 10.1097/01.CCM.0000044505.24727.16.
- Background: PubMed 15891344Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viviand X, Martin C. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severely brain-injured patients. Crit Care Med. 2005 May;33(5):1109-13. doi: 10.1097/01.ccm.0000162491.26292.98.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Ambroise MONTCRIOL, MD principal investigator
Direction Centrale du Service de Santé des Armées
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Ketamine and Sufentanil in people with Head Trauma, run by Pierre-Julien CUNGI at 1 site in France.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 10 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 5 Sep 2014. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in France. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Ambroise MONTCRIOL, MD (0483162358 ext. 0033, ambroise.montcriol@free.fr), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
brain glutamate concentrations (time frame: H0-H12, H12-H24, H24-H36 and H36-H48). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02232347, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 5 Sep 2014.