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Carbamazepine

Carbamazepine is a widely used anticonvulsant medication effective in the treatment of epilepsy, neuropathic pain, and bipolar disorder.
It works by stabilizing the inactivated state of sodium channels, reducing neuronal excitability.
Carbamazepine is known for its complex pharmacokinetics, with significant individual variability in absorption, metabolism, and dosing requirements.
Monitoring of serum levels is often necessary to optimize therapeutic effects and minimize adverse effects such as drowsiness, ataxia, and hyponatremia.
Researchers investigating carbamazepine's mechanisms of action, clinical applications, and pharmacologic properties can leverage PubCompare.ai's AI-powered protocol comparisons to navigate the vast literature and identify the most effective research strategies.

Most cited protocols related to «Carbamazepine»

1
Metabolic Side Effects of Antipsychotics
Cited 9 times
The meta-analysis was conducted and reported according to recommendations of the Meta-analysis of Observational Studies in Epidemiology (MOOSE) group [36] (link). A review protocol was construed following the MOOSE guidelines. This was not published but only for internal use of this study.
A PubMed and Embase search was conducted for articles on metabolic side effect profiles of antipsychotic medication. The search term used was: ((“weight gain” OR “BMI” OR “7% weight”) AND (chlorpromazine OR haloperidol OR bromperidol OR fluphenazine OR zuclopenthixol OR pentixol OR flupentixol OR levopromazine OR perphenazine OR pimozide OR penfluridol OR sulpiride OR amisulpride OR amoxapine OR asenapine OR aripiprazole OR blonanserine OR clozapine OR iloperidone OR melperone OR olanzapine OR risperidone OR paliperidone OR quetiapine OR sertindole OR lurasidone OR ziprasidone)) NOT (addition OR additive OR adjunctive OR augmentation OR lithium OR valproate OR carbamazepine OR metformin OR topiramate OR ramelteon OR rimonabant OR modafinil OR sibutramine OR genetics OR pharmacokinetics OR vomiting OR nausea OR review OR “cognitive behavioural therapy” OR “cognitive behavioral therapy” OR delirium OR steroids OR ropinirole OR sleep OR “brain volume”)
Limits Activated: Humans, Clinical Trial, Randomized Controlled Trial, Clinical Trial, Phase IV, Controlled Clinical Trial, English, German, All Adult: 18+ years, Publication Date from 1999/01/01 to 2011/12/31.
Bak M., Fransen A., Janssen J., van Os J, & Drukker M. (2014). Almost All Antipsychotics Result in Weight Gain: A Meta-Analysis. PLoS ONE, 9(4), e94112.
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Publication 2014
Adult Amisulpride Amoxapine Antipsychotic Agents Aripiprazole asenapine Brain bromperidol Carbamazepine Chlorpromazine Clozapine Cognitive Therapy Delirium Drug Kinetics Drug Reaction, Adverse Flupenthixol Fluphenazine Haloperidol Homo sapiens iloperidone Lithium Lurasidone Metformin Methotrimeprazine metylperon Modafinil Nausea Olanzapine Paliperidone Penfluridol Perphenazine Pimozide Quetiapine ramelteon Rimonabant Risperidone ropinirole sertindole sibutramine Sleep Steroids Sulpiride Topiramate Valproate ziprasidone Zuclopenthixol
2
Anticonvulsant Doses in Neonatal Rats
Cited 9 times
The drug doses used fell within the anticonvulsant range in neonatal rats (Kubova and Mares, 1991; Stankova et al., 1992; Kubová and Mares, 1993). For phenobarbital, the dose selected (75mg/kg) was just below the dose (80mg/kg) that was found to provided complete protection against pentylenetetrazole (PTZ)- induced seizures (both minimal and maximal) in P7 rat pups. (Kubova and Mares, 1991). This dose of phenobarbital was in the middle of the effective dose range previously reported for induction of neuronal apoptosis (Bittigau et al., 2002 (link)). For phenytoin, the dose selected (50mg/kg) was within the range (30–60 mg/kg) that reduced the frequency of PTZ seizures in P7 rats (Stankova et al., 1992) and corresponded to the upper end of the dose range previously reported to induce neuronal apoptosis at P7 (Bittigau et al., 2002 (link)). The dose of carbamazepine used (100mg/kg) was equivalent to twice the highest dose previously shown to protect against maximal PTZ seizures in P7 rats (Kubova and Mares, 1993). Despite the fact that this is a high dose of carbamazepine, this dose previously was found not to cause significant neuronal apoptosis in P7 rat pups (Kim et al., 2007 (link)). Pups were injected (i.p.) with sodium phenobarbital in saline (75mg/kg, n=8, Sigma), phenytoin (sodium diphenylhydantoin) in alkalinized saline (pH 10, 50mg/kg, n=10, Sigma), or a suspension of carbamazepine (100mg/kg, n=6, Sigma) in saline containing 1.0% Tween 80 (Sigma). Control groups received equivalent volumes of vehicle (0.01ml/g body weight, n=11). Treatments occurred on P7, 24h before sacrifice as in prior studies (Bittigau et al., 2002 (link); Kim et al., 2007a (link), 2007b (link)).
Forcelli P.A., Kim J., Kondratyev A, & Gale K. (2011). Brief Communication: Pattern of antiepileptic drug induced cell death in limbic regions of the neonatal rat brain. Epilepsia, 52(12), e207-e211.
Publication 2011
Anticonvulsants Apoptosis Body Weight Carbamazepine Infant, Newborn Neurons Pentylenetetrazole Pharmaceutical Preparations Phenobarbital Phenytoin Phenytoin Sodium Saline Solution Seizures Sodium, Phenobarbital Tween 80
3
Acute Efficacy of Intravenous Ketamine in Treatment-Resistant Depression
Cited 8 times
This was a double-blind, placebo-controlled study of the acute efficacy of IV ketamine or placebo added to ongoing antidepressant therapy (ADT) in the treatment of major depressive disorder (MDD) adults with TRD. Following a washout period for patients on prohibited psychotropic agents, 99 eligible subjects were randomly assigned to one of five 40-minute infusion arms in a 1:1:1:1:1 fashion: a single dose of ketamine 0.1 mg/kg (n=18), a single dose of ketamine 0.2 mg/kg (n=20), a single dose of ketamine 0.5 mg/kg (n=22), a single dose of ketamine 1.0 mg/kg (n=20), and a single dose of midazolam 0.045 mg/kg (active placebo) (n=19) (see Figure 1), to minimize the unblinding risk due to AEs, as in Murrough et al16 (link). Prior to randomization, patients were grouped by BMI (Group I: BMI ≤30; Group II: BMI >30), and were block randomized into each arm of the study, with the mg/Kg ratio being maintained across all BMIs. The primary endpoint assessments were carried out over 3 days and all subjects were followed for 30 days to examine the benefit durability (see Figure 1).
The study assessments were performed at Days 0, 1, 3, 5, 7, 14, and 30 to assess the safety and efficacy of all doses of ketamine compared to active placebo therapy in depressed patients demonstrating an inadequate response to at least 2 adequate ADTs during the current major depressive episode (TRD). This report focuses on the outcome during the acute phase of the study (Days 0 through 3). This trial was conducted across six U.S. academic sites (Massachusetts General Hospital, Baylor College of Medicine/Michael E. Debakey VA Medical Center, Icahn School of Medicine at Mount Sinai, Stanford University School of Medicine, University of Texas Southwestern, and Yale University), according to the U.S. FDA guidelines and Declaration of Helsinki. IRB- and NIMH DSMB-approved written informed consent was obtained from all patients.
All enrolled subjects were male and female outpatients between the ages of 18–70 years old with a diagnosis of MDD in a current depressive episode of at least eight week-duration (as defined by the DSM-IV-TR™). The diagnosis of MDD was supported by the Structured Clinical Interview for DSM-IV (SCID-I/P). Furthermore, all subjects had TRD, defined as failure to achieve a subjective satisfactory response (e.g., less than 50% improvement of depression symptoms) to at least two adequate treatment courses during the current depressive episode (including the current ADT). All study participants with MDD were required to be on a stable (for at least 4 weeks) and adequate (according to the MGH Antidepressant Treatment Response Questionnaire or ATRQ) dose of ongoing ADT, with a total treatment duration of at least 8 weeks. Concurrent hypnotic therapy was allowed if the therapy had been stable for at least 4 weeks prior to screening and was expected to remain stable during the study. Patients were also allowed to continue treatment with benzodiazepines used for anxiety if therapy had been stable for at least 4 weeks prior to screening and expected to remain stable during the study. Patients on exclusionary concomitant psychotropic medications (e.g., opioids, tramadol, valproic acid, lamotrigine, carbamazepine, barbiturates, eszopiclone, stimulants, NMDA receptor antagonists such as memantine), were included only if they had been free of the exclusionary medication post-taper for five half-lives within the maximum screening period (28 days). Furthermore, subjects could be in concurrent psychotherapy, if stable. All subjects had a Montgomery Asberg Depression Rating Scale17 (link) (MADRS) score ≥20 at both the screen and baseline visits. All included patients were required to have a BMI between 18–35 kg/m2.
Major exclusion criteria were as follows: Failure to achieve satisfactory response (e.g., less than 50% improvement of depression symptoms) to >7 treatment courses of a therapeutic dose of an ADT of at least 8 weeks duration in the current major depressive episode, MADRS total score <20 at screening or baseline; a primary Axis I disorder other than MDD; current substance use disorder (abuse or dependence), with the exception of nicotine dependence, within 6 months prior to screening; and any history of ketamine or PCP drug use. All subjects underwent urine drug testing at screening. Other major exclusion criteria included a history of bipolar disorder, schizophrenia or schizoaffective disorders, or any history of psychotic symptoms in the current or previous depressive episodes. Furthermore, previous participants in research studies involving glutamatergic agents for depression were also excluded.
Following the in-person screen, the diagnosis and adequacy of treatment was confirmed by remote, independent raters from the Massachusetts General Hospital (MGH) Clinical Trials Network and Institute (CTNI), via a teleconference administration of the Mood Disorders module of the SCID-I/P, MADRS, and the MGH ATRQ.
Fava M., Freeman M.P., Flynn M., Judge H., Hoeppner B.B., Cusin C., Ionescu D.F., Mathew S.J., Chang L.C., Iosifescu D.V., Murrough J., Debattista C., Schatzberg A.F., Trivedi M.H., Jha M.K., Sanacora G., Wilkinson S.T, & Papakostas G.I. (2018). Double-blind, placebo-controlled, dose-ranging trial of intravenous ketamine as adjunctive therapy in treatment-resistant depression (TRD). Molecular Psychiatry, 25(7), 1592-1603.
Publication 2018
Adult antagonists Antidepressive Agents Anxiety Barbiturates Benzodiazepines Bipolar Disorder Carbamazepine Central Nervous System Stimulants Depressive Symptoms Diagnosis Drug Abuse Epistropheus Eszopiclone Glutamate Agents Hypnotics Ketamine Lamotrigine Males Memantine Mental Disorders Midazolam Mood Disorders N-Methyl-D-Aspartate Receptors Nicotine Dependence Opioids Outpatients Patients Pharmaceutical Preparations Placebos Psychotherapy Psychotropic Drugs Safety Schizoaffective Disorder Schizophrenia Substance Use Disorders Tramadol Unipolar Depression Urinalysis Urine Valproic Acid Woman
4
Hyperthermia-Induced Seizures in Scn1a+/- Mice
Cited 7 times
Hyperthermia‐induced seizure experiments were conducted in Scn1a+/− mice at age postnatal day 14‐16 (P14‐16) using a rodent temperature regulator (TCAT‐2DF, Physitemp Instruments, Inc, Clifton, NJ) reconfigured with a Partlow 1160 + controller (West Control Solutions, Brighton, UK) connected to a heat lamp and RET‐3 rectal temperature probe. Fifteen minutes prior to the target experimental (post‐dose) time point for each drug, the rectal probe was inserted. Mice acclimated to the temperature probe for 5 min before the hyperthermia protocol was started. Mouse core body temperature was elevated 0.5°C every 2 min until the onset of the first clonic convulsion with loss of posture or until 42.5°C was reached. Mice that reached 42.5°C were held at temperature for 3 min. If no seizure occurred during the hold period, the mouse was considered seizure‐free. After thermal induction procedure, plasma samples were isolated as described above and stored at −80°C until assayed. Threshold temperatures were compared using the time to event analysis (logrank Mantel‐Cox), and P < 0.05 was considered statistically significant. No significant sex differences were observed, so groups were collapsed across sex.
Experimental time points were based on previously determined time‐to‐peak plasma and brain concentrations or effect from the literature or our pharmacokinetic studies. Experimental time points used were as follows: 40 min‐ levetiracetam; 45 min‐ carbamazepine, lamotrigine, phenobarbital; 90 min‐ stiripentol, clobazam, topiramate; 120 min phenytoin.20, 21, 22, 23, 24 Valproic acid was administered after the 5 min acclimation period.25, 26 Matched vehicle controls were run for each experimental time point. Vehicle A (saline) was administered at 0, 40, 45, and 90 min. No statistical difference was identified between the four time points and all vehicle A‐treated mice were combined into one group. Vehicles B (0.5% methylcellulose), C (5% hydroxypropyl‐β‐cyclodextrin), and D (vegetable oil) were administered at 120, 45, and 90 min, respectively.
Hawkins N.A., Anderson L.L., Gertler T.S., Laux L., George AL J.r, & Kearney J.A. (2017). Screening of conventional anticonvulsants in a genetic mouse model of epilepsy. Annals of Clinical and Translational Neurology, 4(5), 326-339.
Publication 2017
Acclimatization ARID1A protein, human Brain Carbamazepine Clobazam Clonic Seizures Cyclodextrins Fever Hypromellose Lamotrigine Levetiracetam Methylcellulose Mice, House Pharmaceutical Preparations Phenobarbital Phenytoin Plasma Rectum Rodent Saline Solution Seizures stiripentol Topiramate Valproic Acid Vegetable Oils
5
Carbamazepine Release Kinetics from Chewable Tablets
Cited 6 times
The release kinetics of carbamazepine from the experimental chewable tablets containing the CBZ-β-CD inclusion complex were performed on a DT 800H dissolution tester (Erweka, Langen, Germany). The dissolution test was performed using the USP 32 specifications [29 ], with the Apparatus 2 (paddles) at 75 rpm and 900 mL of 1.0% sodium lauryl sulfate (LSS) aqueous solution at 37.0 ± 0.5 °C, as dissolution medium.
Since the CBZ-β-CD inclusion complex was formulated into chewable tablet, a second dissolution medium, simulating the physical–chemical properties of saliva, was also tested. The final pH of this medium, which contains 8 g/L NaCl, 0.19 g/L KH2PO4, 2.38 g/L Na2HPO4, is 6.8 [30 (link),31 (link)]. Both the experiments in 1% LSS and in simulated saliva were run on 12 tablets. Samples (2 mL) were removed after 5, 10, 15, 30, 45 and 60 min in a glass syringe, filtered through a 0.45-µm Teflon® filter, and diluted 1:10 with methanol. Quantification of the released carbamazepine was performed using an HPLC method, with UV detection at 285 nm.
Dissolution profiles were compared using the f2 similarity factor [32 ]: f2=50log1+∑i=1pxti¯−xri¯2P−1/2×100
where ri and ti are the average percentage of carbamazepine dissolved at a specific time from the reference and test products, respectively, and P is number of measured time points used to evaluate the amount of dissolved carbamazepine.
In order to evaluate the mechanism of the carbamazepine release kinetics, dissolution data were fitted to different kinetic models: zero order, first-order, Higuchi, Korsmeyer–Peppas and Weibull [33 (link),34 (link),35 (link),36 (link)].
Musuc A.M., Anuta V., Atkinson I., Sarbu I., Popa V.T., Munteanu C., Mircioiu C., Ozon E.A., Nitulescu G.M, & Mitu M.A. (2021). Formulation of Chewable Tablets Containing Carbamazepine-β-cyclodextrin Inclusion Complex and F-Melt Disintegration Excipient. The Mathematical Modeling of the Release Kinetics of Carbamazepine. Pharmaceutics, 13(6), 915.
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Publication 2021
Carbamazepine chemical properties High-Performance Liquid Chromatographies Kinetics Methanol Physical Examination Saliva Sodium Chloride Sulfate, Sodium Dodecyl Syringes Teflon

Most recents protocols related to «Carbamazepine»

1
Chronic Pain after Elderly Arthroplasty
Elderly patients who underwent lower extremity arthroplasty in Drum Tower Hospital Affiliated to Nanjing University Medical School from September 2020 to March 2021 were selected and followed up for postoperative pain assessment using the numerical rating scale NRS. The elderly osteoarthritis patients selected were all caused by joint degeneration rather than fractures or necrosis caused by other reasons. They were performed operations by the same group of doctors and operation method. All patients signed informed consent and were authorized by the ethics committee of Drum Tower Hospital Affiliated to Nanjing University Medical School (Nanjing, China, No. 2019-270-02). Inclusion criteria: (1) Age ≥ 65 years old; (2) American Society of Anesthesiologists (ASA) classification II–III; (3) Patients undergoing lower extremity arthroplasty; (4) Operation duration ≥ 60 min; (5) Patients recorded in electronic medical record system; (6) Patients agreed to participate in the study and signed the informed consent. Exclusion criteria: (1) With gene deficiency disease; (2) Having history of opioid abuse; (3) Using drugs that induce or inhibit liver isoenzymes (such as carbamazepine, quinidine, ketoconazole, etc.) in 4 weeks before operation; (4) Combined with peripheral neuropathy and psychiatric history, chronic pain and long-term opioid use history; (5) With poor body conditions affecting the perioperative pain evaluation; (6) Patients can’t cooperate and communicate with.
The patient's NRS score being ≥ 4 on the 90th day after operation was identified as having severe CPSP. A total of 10 patients were judged to have severe CPSP (group A). 10 patients hospitalized in the same period without chronic postsurgical pain (NRS score = 0 on the 90th day after operation) were randomly selected as the control group (group B).
Xu R., Jin Y., Tang S., Wang W., Sun Y.E., Liu Y., Zhang W., Hou B., Huang Y, & Ma Z. (2023). Association between single nucleotide variants and severe chronic pain in older adult patients after lower extremity arthroplasty. Journal of Orthopaedic Surgery and Research, 18, 184.
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Publication 2023
Abuse, Opioid Aged Anesthesiologist Arthroplasty Carbamazepine Cardiac Arrest Chronic Pain Deficiency Diseases Degenerative Arthritides Ethics Committees, Clinical Fracture, Bone Genes Human Body Isoenzymes Ketoconazole Liver Lower Extremity Necrosis Opioids Pain Measurement Patients Peripheral Nervous System Diseases Pharmaceutical Preparations Physicians Postoperative Pain, Chronic Quinidine
2
HPLC-Based Protein Binding Estimation
Retention times of the analytes were measured with Shimadzu HPLC system on the CHIRALPAK®HAS stationary phase (50 × 3 mm, 5 μm, Chiral Technologies, DAICEL Group, Europe SAS, France). The mobile phase A consisted of 50 mM aqueous ammonium acetate buffer (pH 7.4) and phase B of 2-propanol according to Valko et al.65 (link) Analysis was performed at prolonged 1 mL min−1 flow rate in the linear gradient. Retention capacity factors (k′) were calculated by using DMSO or a substance with 0% HAS binding for systems' dead time (Rt0). The system was calibrated by injecting the reference compounds: acetylsalicylic acid (CAS 69-72-7), betamethasone (CAS 378-44-9), budesonide (CAS 5133-22-3), carbamazepine (CAS 298-46-4), cimetidine (CAS 51481-61-9), ciprofloxacin (CAS 85721-33-1), indomethacin (CAS 53-86-1), isoniazid (CAS 54-85-3), metronidazole (CAS 443-48-1), nicardipine (CAS 55985-32-5), nizatidine (CAS 76963-41-2) and warfarin (CAS 81-81-2) obtained from Sigma-Aldrich, diclofenac (CAS 15307-86-5) from EMD Chemicals Inc., flumazenil (CAS 78755-81-4) from ABX and ketoprofen (CAS 22071-15-4) from LKT Labs. The logarithmic capacity factors of the references' Rt (log(k′)) on the HSA column were plotted against the %PPB values from literature. The slope and the intercept were used to convert the log(k′) of the compounds (6a, c, f, h, m–o) to %PPB using the regression equation.66 (link)
Dzedulionytė K., Fuxreiter N., Schreiber-Brynzak E., Žukauskaitė A., Šačkus A., Pichler V, & Arbačiauskienė E. (2023). Pyrazole-based lamellarin O analogues: synthesis, biological evaluation and structure–activity relationships. RSC Advances, 13(12), 7897-7912.
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Publication 2023
ammonium acetate Aspirin Betamethasone Budesonide Buffers Carbamazepine Cimetidine Ciprofloxacin Diclofenac Flumazenil High-Performance Liquid Chromatographies Indomethacin Isoniazid Ketoprofen Metronidazole Nicardipine Nizatidine Propanols Retention (Psychology) Sulfoxide, Dimethyl Warfarin
3
Preclinical Evaluation of Antiepileptic Drugs
C57/BL mice (male, 22–26 g) were supplied by SiBeiFu (Beijing) Biotechnology Co., Ltd. (China). Mice were raised at 24 °C with 12 h light/dark cycles, which is accessible to food and water freely. Mice were adapted for 7 days to before the experiments. All the experiments, especially epileptic seizure score experiments, antiepileptic drug therapy experiments, enzyme activity test, CN inhibitor assay, CNA knockdown experiments and Nissl staining tests were performed with the standard of double-blinded way. In antiepileptic drug therapy experiment, the mice were injected with tutin (2 mg/kg, i.p.) after oral administration of MK-801 (0.5 mg/kg), Retigabine (60 mg/kg), Diazepam (3 mg/kg), Carbamazepine (20 mg/kg). In the antiepileptic evaluation experiment of martentoxin, martentoxin (0.05 μg in 1 μL saline) was microinjected into the region of hippocampus, and then the mice were injected with tutin. In CN inhibitor assay, CN inhibitor FK506 (0.5 mg/kg, i.p.) was administrated to mice 1 h before tutin injection. The animal trails were carried out following the rules of the Institutional Animal Care and Use Committee of Peking Union Medical College. All procedures were carried out according to “three Rs” principle.
Han Q.T., Yang W.Q., Zang C., Zhou L., Zhang C.J., Bao X., Cai J., Li F., Shi Q., Wang X.L., Qu J., Zhang D, & Yu S.S. (2023). The toxic natural product tutin causes epileptic seizures in mice by activating calcineurin. Signal Transduction and Targeted Therapy, 8, 101.
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Publication 2023
Administration, Oral Animals Antiepileptic Agents Biological Assay Carbamazepine Diazepam ezogabine FK-506 Food Institutional Animal Care and Use Committees Males Mice, House Mice, Inbred C57BL MK-801 Pharmacotherapy Saline Solution Seahorses Seizures Test, Clinical Enzyme Therapeutics TNFSF10 protein, human tutin
4
Anticonvulsant Drug Treatment for Seizures
Mice were randomly assigned to each group. We used 2 classic anti-epilepsy drugs: carbamazepine (CBZ) and valproic acid (VPA). The treatments were initiated on day 10 after Dox withdrawal from the drinking water, the time-point at which the seizure activity began to become obvious. CBZ was dissolved in DMSO and diluted in 0.9% NaCl. VPA was directly added to the drinking water of both control and transgenic groups. The dosages were based on previous studies43 (link). For CBZ, we increased the dose daily to mimic the clinical application (Day 10: 5 mg/kg; Day 11: 10 mg/kg; Day 12: 15 mg/kg; Day 13: 20 mg/kg; Day 14: 25 mg/kg). For VPA, to reach 500 mg/kg per day, we decided the VPA concentration in the drinking water on the average daily volume of water consumed (around 5 mL per day).
Wang Z., Li Q., Kolls B.J., Mace B., Yu S., Li X., Liu W., Chaparro E., Shen Y., Dang L., del Águila Á., Bernstock J.D., Johnson K.R., Yao J., Wetsel W.C., Moore S.D., Turner D.A, & Yang W. (2023). Sustained overexpression of spliced X-box-binding protein-1 in neurons leads to spontaneous seizures and sudden death in mice. Communications Biology, 6, 252.
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Publication 2023
Animals, Transgenic Antiepileptic Agents Carbamazepine Mice, House Normal Saline Pharmaceutical Preparations Seizures Sulfoxide, Dimethyl Valproic Acid
5
Microvascular Decompression for Trigeminal Neuralgia
We prospectively studied 57 consecutive patients with TN who underwent MVD surgery between January 2018 and December 2020. Written informed consent was obtained from all patients. The institutional review board approved this cohort study. The authors prepared the manuscript following the Strengthening the Reporting of Observational Studies in Epidemiology guideline.[29 (link)]
Inclusion criteria were a diagnosis of classical TN according to the International Classification of Headache Disorders 3rd edition,[9 ] age 18 years and older, demonstration of neurovascular compression on magnetic resonance imaging, and appropriate medical treatment before MVD. The patients were treated with carbamazepine at an acceptable dose. The patients allergic to carbamazepine were treated with pregabalin or gabapentin, as the regional drug administration approved oxcarbazepine for TN patients. We excluded patients who had undergone surgery for TN previously. We divided the patients into four age groups: those below 60 years, those between 60 and 69 years, those between 70 and 79 years, and those aged 80 years and older. All patients underwent MVD to mobilize the superior cerebellar artery (SCA) and other offending vessels from the trigeminal nerve root.[15 ,28 (link)] The follow-up period for recurrence and complication was 12– 48 months.
The clinical parameters were as follows: age at operation, affected side, neuralgia type, preoperative comorbidity, operative findings of offending vessels, preoperative, and postoperative Barrow Neurological Institute (BNI) pain intensity score I, no trigeminal pain, no medication; II, occasional pain, not requiring medication; III, some pain, adequately controlled with medication; IV, some pain, not adequately controlled with medication; V, severe pain/no pain relief)[24 (link)] and carbamazepine dose, postoperative complications, and recurrence of neuralgia. The offending vessels were classified into four groups: (i) SCA alone (SCA); (ii) SCA and additional vessels (SCA-plus); (iii) non-SCA arterial compressions (other arteries); and (iv) transverse pontine, pontotrigeminal, or other veins (vein).
Yoshizaki W., Fujikawa Y., Torikoshi S., Katayama T., Iwasaki K, & Toda H. (2023). Effects of microvascular decompression on quality-of-life in trigeminal neuralgia patients aged 70 years and older. Surgical Neurology International, 14, 41.
Publication 2023
Age Groups Arteries Blood Vessel Carbamazepine Cerebellum Diagnosis Ethics Committees, Research Fifth Cranial Nerves Gabapentin Headache Disorders Neuralgia Oxcarbazepine Pain Patients Pharmaceutical Preparations Pons Postoperative Complications Pregabalin Recurrence Severity, Pain Tooth Root Veins

Top products related to «Carbamazepine»

1
Carbamazepine by Merck Group
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Carbamazepine is a chemical compound used as a reference standard in analytical testing procedures. It is a white, crystalline powder that is commonly used to verify the accuracy and precision of analytical equipment and methods.
2
Acetonitrile by Merck Group
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Acetonitrile is a colorless, volatile, flammable liquid. It is a commonly used solvent in various analytical and chemical applications, including liquid chromatography, gas chromatography, and other laboratory procedures. Acetonitrile is known for its high polarity and ability to dissolve a wide range of organic compounds.
3
Formic acid by Merck Group
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Formic acid is a colorless, pungent-smelling liquid chemical compound. It is the simplest carboxylic acid, with the chemical formula HCOOH. Formic acid is widely used in various industrial and laboratory applications.
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Methanol by Thermo Fisher Scientific
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5
Methanol by Merck Group
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Methanol is a clear, colorless, and flammable liquid that is widely used in various industrial and laboratory applications. It serves as a solvent, fuel, and chemical intermediate. Methanol has a simple chemical formula of CH3OH and a boiling point of 64.7°C. It is a versatile compound that is widely used in the production of other chemicals, as well as in the fuel industry.
6
Acetonitrile by Thermo Fisher Scientific
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Acetonitrile is a highly polar, aprotic organic solvent commonly used in analytical and synthetic chemistry applications. It has a low boiling point and is miscible with water and many organic solvents. Acetonitrile is a versatile solvent that can be utilized in various laboratory procedures, such as HPLC, GC, and extraction processes.
7
Phenytoin by Merck Group
Sourced in United States, Germany, Poland, India, United Kingdom
Phenytoin is a laboratory reagent used in the analysis and identification of pharmaceutical and biological samples. It is a crystalline solid compound that is commonly used as a standard for high-performance liquid chromatography (HPLC) and other analytical techniques. Phenytoin is a widely recognized and well-characterized compound that is often used as a reference material in the pharmaceutical and scientific research industries.
8
Diclofenac by Merck Group
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Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) that is used as a pain reliever and anti-inflammatory agent. It is a commonly used pharmaceutical ingredient in various lab equipment and medical products.
9
Ibuprofen by Merck Group
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Ibuprofen is a laboratory-grade chemical compound used as a reference standard in analytical testing. It is a white, crystalline solid with a melting point of around 78°C. Ibuprofen is a common non-steroidal anti-inflammatory drug (NSAID) and is often used as a calibration standard for the identification and quantification of pharmaceutical and biological samples.
10
Phenobarbital by Merck Group
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Phenobarbital is a pharmaceutical product manufactured by Merck Group. It is a barbiturate compound commonly used as a sedative and anticonvulsant medication. The core function of Phenobarbital is to depress the central nervous system and induce a calming effect.

More about "Carbamazepine"

Carbamazepine is a widely used anticonvulsant medication, also known as an antiepileptic drug (AED), that is effective in the treatment of various neurological and psychiatric conditions.
It is commonly prescribed for the management of epilepsy, neuropathic pain, and bipolar disorder.
The mechanism of action of carbamazepine involves stabilizing the inactivated state of sodium channels, which reduces neuronal excitability and helps to control seizures and other neurological symptoms.
Carbamazepine is known for its complex pharmacokinetics, with significant individual variability in absorption, metabolism, and dosing requirements.
Monitoring of serum levels is often necessary to optimize therapeutic effects and minimize adverse effects such as drowsiness, ataxia, and hyponatremia.
When investigating carbamazepine's mechanisms of action, clinical applications, and pharmacologic properties, researchers can leverage PubCompare.ai's AI-powered protocol comparisons to navigate the vast literature, including scientific publications, preprints, and patents.
This tool can help identify the most effective research strategies and optimize the use of carbamazepine.
In addition to carbamazepine, other relevant substances and compounds may be of interest, such as acetonitrile, formic acid, methanol, phenytoin, diclofenac, ibuprofen, and phenobarbital.
These substances may be used in analytical techniques, drug interactions, or as comparators in carbamazepine research.
By incorporating insights from these related terms, researchers can gain a more comprehensive understanding of the pharmacological properties and applications of carbamazepine.