The Experts below are selected from a list of 735 Experts worldwide ranked by ideXlab platform
Robert Kronstrand - One of the best experts on this subject based on the ideXlab platform.
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Concentration-time profiles of gamma-hydroxybutyrate in blood after recreational doses are best described by zero-order rather than first-order kinetics.
Journal of analytical toxicology, 2009Co-Authors: Alan Wayne Jones, Arne Eklund, Robert KronstrandAbstract:The recreational drug gamma-hydroxybutyrate (GHB) has a short plasma elimination half-life (t(1/2)) reported to be about 30-50 min. However, this represents a terminal half-life and therefore might not necessarily apply after large (abuse) doses are taken. Clinical studies with Sodium Oxybate (Sodium salt of GHB) suggest that zero-order rather than first-order kinetics are more appropriate to describe post-peak concentration-time (C-T) profiles. We report the case of a 23-year-old male found unconscious by the police and a blood sample contained 100 mg/L GHB and 0.14 g% ethanol. On regaining consciousness the man admitted drinking alcohol about 6 h earlier but claimed that his drink must have been spiked with GHB. The police wanted to know how much GHB had been administered to account for the man's clinical condition. A back-calculation for 6 h, assuming a GHB half-life of 40 min, gives a very high concentration in blood of approximately 900 mg/L, which would probably have proven fatal. Back-calculating using zero-order kinetics and a proposed elimination rate of 18 mg/L per hour leads to a GHB concentration of 208 mg/L, which is much more realistic. Toxicologists should not arbitrarily apply the principles of first-order kinetics after abuse doses of drugs, when zero-order or saturation kinetics (Michaelis-Menten) are more appropriate.
Alan Wayne Jones - One of the best experts on this subject based on the ideXlab platform.
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Concentration-time profiles of gamma-hydroxybutyrate in blood after recreational doses are best described by zero-order rather than first-order kinetics.
Journal of analytical toxicology, 2009Co-Authors: Alan Wayne Jones, Arne Eklund, Robert KronstrandAbstract:The recreational drug gamma-hydroxybutyrate (GHB) has a short plasma elimination half-life (t(1/2)) reported to be about 30-50 min. However, this represents a terminal half-life and therefore might not necessarily apply after large (abuse) doses are taken. Clinical studies with Sodium Oxybate (Sodium salt of GHB) suggest that zero-order rather than first-order kinetics are more appropriate to describe post-peak concentration-time (C-T) profiles. We report the case of a 23-year-old male found unconscious by the police and a blood sample contained 100 mg/L GHB and 0.14 g% ethanol. On regaining consciousness the man admitted drinking alcohol about 6 h earlier but claimed that his drink must have been spiked with GHB. The police wanted to know how much GHB had been administered to account for the man's clinical condition. A back-calculation for 6 h, assuming a GHB half-life of 40 min, gives a very high concentration in blood of approximately 900 mg/L, which would probably have proven fatal. Back-calculating using zero-order kinetics and a proposed elimination rate of 18 mg/L per hour leads to a GHB concentration of 208 mg/L, which is much more realistic. Toxicologists should not arbitrarily apply the principles of first-order kinetics after abuse doses of drugs, when zero-order or saturation kinetics (Michaelis-Menten) are more appropriate.
Thomas Foltynie - One of the best experts on this subject based on the ideXlab platform.
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Sodium Oxybate AS A TREATMENT FOR DBS–RESISTANT, ALCOHOL–RESPONSIVE POST–ANOXIC MYOCLONUS
Journal of Neurology Neurosurgery & Psychiatry, 2013Co-Authors: Joshua Kahan, Zinovia Kefalopoulou, James Gratwicke, Iciar Aviles-olmos, Ludvic Zrinzo, Marwan Hariz, Patricia Limousin, Thomas FoltynieAbstract:Myoclonic jerks are sudden shock–like involuntary movements, either manifesting as a brief contraction of a group of muscles (positive) or cessation of muscle activity (negative), driven by aberrant activity in one of the cortex, subcortical regions, brainstem or spinal cord. Its aetiology is variable and can occur physiologically, in a primary myoclonic syndrome (myoclonus–dystonia), or as part of an epilepsy (Progressive myoclonic epilepsy) or neurodegenerative syndrome (Alzheimer9s disease, multiple systems atrophy). Myoclonus can also occur secondary to hypoxic brain injury either in an acute (myoclonic status epilepticus) or a chronic form, eponymously titled Lance–Adams syndrome (LAS). LAS is characterised by a non–progressive generalised myoclonus with added seizures and ataxia. There is no curative management strategy, only symptomatic relief. A multidisciplinary approach involving medical, physiotherapy, speech and occupational therapy achieves the best holistic outcomes for patients. Case studies suggest certain antiepileptic agents may alleviate symptoms, but combinations are often required, and the most effective options have sedative side effects. A subset of cases have marked alcohol responsiveness that can lead to dependence. A number of experimental treatment options have been proposed including deep brain stimulation (DBS) and Sodium Oxybate, a Sodium salt of gamma–Hydroxybutyrate. In what follows, a patient with an eleven year history of the LAS is presented and the experimental therapeutics explored, concluding with a recent trial of Sodium Oxybate. Sodium Oxybate was well tolerated and produced improvements in the patient9s symptoms and perceived disability. This case highlights the difficulties of managing chronic myoclonic conditions and suggests Sodium Oxybate may be a useful treatment option in these patients.
Arne Eklund - One of the best experts on this subject based on the ideXlab platform.
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Concentration-time profiles of gamma-hydroxybutyrate in blood after recreational doses are best described by zero-order rather than first-order kinetics.
Journal of analytical toxicology, 2009Co-Authors: Alan Wayne Jones, Arne Eklund, Robert KronstrandAbstract:The recreational drug gamma-hydroxybutyrate (GHB) has a short plasma elimination half-life (t(1/2)) reported to be about 30-50 min. However, this represents a terminal half-life and therefore might not necessarily apply after large (abuse) doses are taken. Clinical studies with Sodium Oxybate (Sodium salt of GHB) suggest that zero-order rather than first-order kinetics are more appropriate to describe post-peak concentration-time (C-T) profiles. We report the case of a 23-year-old male found unconscious by the police and a blood sample contained 100 mg/L GHB and 0.14 g% ethanol. On regaining consciousness the man admitted drinking alcohol about 6 h earlier but claimed that his drink must have been spiked with GHB. The police wanted to know how much GHB had been administered to account for the man's clinical condition. A back-calculation for 6 h, assuming a GHB half-life of 40 min, gives a very high concentration in blood of approximately 900 mg/L, which would probably have proven fatal. Back-calculating using zero-order kinetics and a proposed elimination rate of 18 mg/L per hour leads to a GHB concentration of 208 mg/L, which is much more realistic. Toxicologists should not arbitrarily apply the principles of first-order kinetics after abuse doses of drugs, when zero-order or saturation kinetics (Michaelis-Menten) are more appropriate.
Joshua Kahan - One of the best experts on this subject based on the ideXlab platform.
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Sodium Oxybate AS A TREATMENT FOR DBS–RESISTANT, ALCOHOL–RESPONSIVE POST–ANOXIC MYOCLONUS
Journal of Neurology Neurosurgery & Psychiatry, 2013Co-Authors: Joshua Kahan, Zinovia Kefalopoulou, James Gratwicke, Iciar Aviles-olmos, Ludvic Zrinzo, Marwan Hariz, Patricia Limousin, Thomas FoltynieAbstract:Myoclonic jerks are sudden shock–like involuntary movements, either manifesting as a brief contraction of a group of muscles (positive) or cessation of muscle activity (negative), driven by aberrant activity in one of the cortex, subcortical regions, brainstem or spinal cord. Its aetiology is variable and can occur physiologically, in a primary myoclonic syndrome (myoclonus–dystonia), or as part of an epilepsy (Progressive myoclonic epilepsy) or neurodegenerative syndrome (Alzheimer9s disease, multiple systems atrophy). Myoclonus can also occur secondary to hypoxic brain injury either in an acute (myoclonic status epilepticus) or a chronic form, eponymously titled Lance–Adams syndrome (LAS). LAS is characterised by a non–progressive generalised myoclonus with added seizures and ataxia. There is no curative management strategy, only symptomatic relief. A multidisciplinary approach involving medical, physiotherapy, speech and occupational therapy achieves the best holistic outcomes for patients. Case studies suggest certain antiepileptic agents may alleviate symptoms, but combinations are often required, and the most effective options have sedative side effects. A subset of cases have marked alcohol responsiveness that can lead to dependence. A number of experimental treatment options have been proposed including deep brain stimulation (DBS) and Sodium Oxybate, a Sodium salt of gamma–Hydroxybutyrate. In what follows, a patient with an eleven year history of the LAS is presented and the experimental therapeutics explored, concluding with a recent trial of Sodium Oxybate. Sodium Oxybate was well tolerated and produced improvements in the patient9s symptoms and perceived disability. This case highlights the difficulties of managing chronic myoclonic conditions and suggests Sodium Oxybate may be a useful treatment option in these patients.
