ABSTRACT
OBJECTIVE: Warnings of L-carnitine induced seizures are recorded on product monographs and pharmacy databases, without any referenced literature. This medication can potentially improve the hospital course in those patients with valproic acid (VPA) induced hyperammonemic encephalopathy, but may be withheld because of this warning. The goal was to perform an extensive systematic review of the literature to document the incidence of levocarnitine (L-carnitine) induced seizures in those patients on VPA therapy. METHODS: Articles from MEDLINE, BIOSIS, EMBASE, Global Health, Scopus, Cochrane Library, the International Clinical Trials Registry Platform, clinicaltrials.gov (inception to June 2015), and reference lists of relevant articles were searched. The strength of evidence was to be adjudicated using both the Oxford and GRADE methodology by two independent reviewers. RESULTS: We failed to identify a single study implicating L-carnitine supplementation leading to seizures in any patient on VPA therapy. This contradicts all quoted, but unsubstantiated, concerns on product monographs and pharmacy databases related to seizure induction/propagation with L-carnitine supplementation. CONCLUSION: There is no literature available to support claims of L-carnitine induced seizures during supplementation in patients on VPA therapy for seizures. This contradicts quoted, but not referenced, concerns on the product monograph. In patients suffering from hypocarnitinemia or hyperammonemic encephalopathy while on VPA, L-carnitine supplementation can be considered knowing there is no data to support seizure propagation or induction with administration of this supplement.
Subject(s)
Anticonvulsants/therapeutic use , Carnitine/adverse effects , Seizures/chemically induced , Seizures/drug therapy , Valproic Acid/therapeutic use , Databases, Factual/statistics & numerical data , HumansABSTRACT
Background. The goal of our study was to perform a systematic review of the literature to determine the effect that intravenous (IV) lidocaine had on ICP in patients with neurological illness. Methods. All articles are from MEDLINE, BIOSIS, EMBASE, Global Health, Scopus, Cochrane Library, the International Clinical Trials Registry Platform (inception to March 2015). The strength of evidence was adjudicated using both the Oxford and GRADE methodology. Results. Ten original articles were considered for the final review. There were 189 patients studied. Seven studies focused on prophylactic pretreatment with IV lidocaine to determine if there would be an attenuation of ICP spikes during stimulation, with 4 displaying an attenuation of ICP. Three studies focused on a therapeutic administration of IV lidocaine in order to determine ICP reduction effects. All therapeutic studies displayed a reduction in ICP. Conclusions. We cannot make a strong definitive recommendation on the effectiveness of IV lidocaine on the attenuation of ICP spikes during stimulation. There currently exists both Oxford 2b and GRADE B literature to support and refute the attenuation of ICP spikes with IV lidocaine during stimulation. There currently exists Oxford 2b, GRADE B evidence to support ICP reduction with lidocaine when used as a therapeutic agent.
ABSTRACT
1. The influence of (+)-amphetamine, given 1 min after each training session, on the performance of 124 rats in a Lashley III maze was measured every 48 hr.2. The first three injections of the drug significantly improved the learning ability of naive rats.3. With prolonged treatment, (+)-amphetamine strongly impaired the maze performance of these rats.4. The chronic administration of (+)-amphetamine to previously trained rats produced the same adverse effect.5. Amylobarbitone sodium given to previously trained rats 30 min before the training sessions completely blocked the adverse effect of (+)-amphetamine.6. (+)-Amphetamine did not produce impairment of performance when given chronically 30 min before training sessions, to previously trained rats.
