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Books on the topic 'Carbamazepine'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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1

Medenwald, Janet R. Carbamazepine and manic depression : a guide. Rev. ed: Lithium Information Center/Dean Foundation for Health, Research and Education, 1996.

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2

Internationales Carbamazepin Slow-Release Symposium (2nd 1986 Frankfurt am Main). 2. Internationales Carbamazepin Slow-Release Symposium, Frankfurt am Main, Dezember 1986. München: W. Zuckschwerdt, 1988.

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3

Greil, Waldemar. Manic depressive illness: Therapy with carbamazepine : for patients, relatives and therapists. Stuttgart: Thieme, 1996.

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4

McDermott, Elaine Elizabeth. Inositol lipid hydrolysis in the rat hippocampus: Effects of the anticonvulsant carbamazepine. Birmingham: University of Birmingham, 1989.

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5

Johnson, Robert D. False carbamazepine positives due to 10,11-dihydro-10-hydroxycarbamazepine breakdown in the GC/MS injector port. Washington, D.C: Federal Aviation Administration, Office of Aerospace Medicine, 2010.

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6

Parker, Philip M., and James N. Parker. Tegretol: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

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7

1954-, Joffe Russell T., and Calabrese Joseph R, eds. Anticonvulsants in mood disorders. New York: M. Dekker, 1994.

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8

Carbamazepine in affective disorder. CNS (Clinical Neuroscience), 1987.

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9

Cavanna, Andrea E. Carbamazepine, oxcarbazepine, and eslicarbazepine. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198791577.003.0003.

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Carbamazepine is a first-generation antiepileptic drug characterized by a good range of antiepileptic indications, with acceptable risk of interactions in polytherapy. Carbamazepine has a very good behavioural tolerability profile and is in widespread psychiatric use (indication for bipolar disorder—acute mania). Oxcarbazepine and eslicarbazepine are carbamazepine derivatives. Oxcarbazepine is a second-generation antiepileptic drug characterized by a good range of antiepileptic indications, with acceptable risk of interactions in polytherapy. Like carbamazepine, oxcarbazepine has a very good behavioural tolerability profile and potential for widespread psychiatric use. Eslicarbazepine is a third-generation antiepileptic drug for which clinical experience is still limited. Little is known about its positive and negative psychotropic properties and their implications for the management of behavioural symptoms in patients with epilepsy.
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10

Jefferson, James W., and John H. Greist. Carbamazepine & Manic Depression: A Guide. Madison Inst of Medicine, 1996.

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11

M, Emrich H., Schiwy W, and Silverstone Trevor, eds. Carbamazepine and oxcarbazepine in psychiatry. London: Clinical Neuroscience Publishers, 1990.

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12

Woods, Bernadette A. Carbamazepine: Indications, Contraindications and Adverse Effects. Nova Science Publishers, Incorporated, 2017.

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13

Jefferson, James W. Carbamazepine and Bipolar Disorder: A Guide. Madison Inst of Medicine, 2005.

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14

Gallelli, Luca. Carbamazepine: Medical Uses, Pharmacokinetics and Adverse Effects. Nova Science Publishers, Incorporated, 2014.

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15

Bloomer, Denise. The acceptability, stability and bioavailability of carbamazepine oral suspension. 1986.

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16

Love, Nancy G. Demonstrating Advanced Oxidation Coupled with Biodegradation for Removal of Carbamazepine. IWA Publishing, 2012.

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17

Stroebel-Sassim, C., and N. Sassim. Manic-depressive Disease. Thieme Publishing Group, 1996.

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18

Coming Off Psychiatric Drugs: Successful Withdrawal from Neuroleptics, Antidepressants, Lithium, Carbamazepine and Tranquilizers. 2nd ed. Peter Lehmann Publishing, 2002.

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19

Ju, Changqing. Reactive iminoquinone metabolites of indomethacin and carbamazepine: Implications for drug-induced idiosyncratic reactions. 1999.

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20

Bengt, Sternebring, ed. Carbamazepine in the treatment of alcoholics: Workshop, Mariehamn, Finland, October 3-5, 1985. Oslo: Universitetsforlaget, 1987.

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21

Characterization of anti-cytochrome P450 antibodies in patients with carbamazepine hypersensitivity reactions: A mechanistic study. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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22

Keck, Paul E., and Susan L. McElroy. Pharmacological Treatments for Bipolar Disorder. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780199342211.003.0008.

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The majority of clinical trials in patients with bipolar disorders have been conducted in groups with bipolar I illness, although a few trials have included patients with bipolar II disorder. Pharmacological management of bipolar disorder involves the treatment of acute manic, hypomanic, mixed, and depressive episodes, as well as the prevention of further episodes and subsyndromal symptoms. Lithium, divalproex, carbamazepine, haloperidol, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, and asenapine have demonstrated efficacy in the treatment of acute mania in randomized controlled (type 1) trials. Although the pharmacological treatment of acute bipolar depression remains understudied, data from randomized controlled trials indicate that lithium, olanzapine, olanzapine-fluoxetine, quetiapine, lurasidone, tricyclics, monoamine oxidase inhibitors, and fluoxetine have efficacy in this phase of the illness. Lithium, lamotrigine, olanzapine, aripiprazole, quetiapine, and risperidone (long-acting, injectable) have been shown to have efficacy in relapse prevention. Less extensive data suggest that divalproex and carbamazepine are also efficacious for prevention.
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23

Furst, Sylvia Martha. Metabolism of carbamazepine to a reactive intermediate by the myeloperoxidase system of activated neutrophils: a possible mechanism for drug-induced idiosyncratic reactions. 1994.

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24

Walsh, Richard A. “It Has to Be Functional!”. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0026.

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The paroxysmal dyskinesias are a heterogeneous group of rare movement disorders, characterized by the abrupt onset of involuntary hyperkinetic movements with or without trigger factors and of variable duration. Interictal periods are marked by relative normality, although there is evidence for an association between some genotypes and migraine, episodic ataxia, and seizure disorders. Three genes have been identified that are associated with the three most common syndromes; however, these do not account for some cases with an otherwise typical history. The clinical phenotype continues to evolve with increasing characterization of genetically proven cases. Paroxysmal kinesigenic dyskinesia responds well to carbamazepine therapy.
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25

Schmidt, Dieter, and Simon Shorvon. The Pharmaceutical Phoenix Rises. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198725909.003.0003.

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This chapter considers the evolution of drug therapy between 1860 and 1970, a period dominated by five compounds: bromide, phenobarbital, phenytoin, carbamazepine, and valproate. These drugs have changed the lives of people with epilepsy for the better, more perhaps than any other treatment, before or since, and deserve to be celebrated. With the possible exception of phenytoin, the antiepileptic properties of these drugs were detected largely by chance. Each though each was a child of its time, each has had both positive and negative features. These were landmarks in reducing and ameliorating seizures as a symptom of epilepsy, but are not a cure of the disease.
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26

Katz, Rachel, and Robert Beech. Suicide Risk in Bipolar Disorder. Edited by Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari, and Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0005.

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This chapter provides a summary of a landmark study on bipolar disorder, tackling the serious issue of suicidality in this at-risk group of patients. Is there a difference in suicide risk for patients with bipolar disorder who are treated with lithium, divalproex, or carbamazepine? Starting with that question, it describes the basics of the study, including funding, study location, who was studied, how many patients, study design, study intervention, follow-up, endpoints, results, and criticism and limitations. The chapter briefly reviews other relevant studies and information, discusses implications, and concludes with a relevant case that applies the findings from the study to a clinical scenario.
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27

O’Neal, M. Angela. Pain in the Back. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0006.

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This case explores how bone health can be affected by antiepileptic drugs (AEDs), and why this is an important issue in women with epilepsy (WWE). AEDs affect bone health through activation of the cytochrome P450 system in the liver, leading to increased metabolism of vitamin D. The enzyme-inducing AEDs include phenytoin, carbamazepine, phenobarbital, and primidone. Risk factors for osteoporosis include female gender, low body mass, inadequate vitamin D intake, and smoking. The specific AEDs used and the length of treatment confer additional risks. Furthermore, in WWE, risks are magnified related to falls, either from seizures or related to medication toxicity. Screening with bone density and measures to promote bone health are extremely important in these at-risk women.
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28

Calabrese, Joseph R., and Russell T. Joffe. Anticonvulsants in Mood Disorders. Taylor & Francis Group, 1994.

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29

Alshaikh, Jumana T., Shaan Sudhakaran, and Helene Rubeiz. Trigeminal Neuralgia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0002.

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Trigeminal neuralgia is characterized by severe, unilateral, paroxysmal stabbing pain affecting the face in the distribution of one of the divisions of the trigeminal nerve. The episodes of pain are brief and are triggered by innocuous physical stimuli. Typical age of onset is the sixth decade, with a female predominance. The most common cause is neurovascular compression. Other causes include multiple sclerosis and structural abnormalities in the cerebellopontine angle. The diagnosis is made clinically, but MRI can be useful in evaluation of the underlying etiology. First-line pharmacotherapy is carbamazepine or oxcarbazepine. If medical therapy fails, procedural interventions should be considered. From ablations to craniotomy, there is an array of procedural treatments available for trigeminal neuralgia. Patients should be educated on the risks and benefits of each procedure prior to pursuing treatment.
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30

Popovic, Dina, and Eduard Vieta. Evidence-based maintenance treatment of bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0008.

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Due to the episodic and chronic nature of bipolar disorder, maintenance therapy represents a critical part of treatment. However, there is a paucity of studies comparing effectiveness of available long-term treatments. In this chapter, the efficacy and safety of pharmacological treatments for maintenance treatment of bipolar disorder, as deriving from the results of randomized controlled trials, will be critically reviewed. These include second-generation antipsychotics aripiprazole, olanzapine, quetiapine, risperidone long-acting injection, ziprasidone, paliperidone, and mood stabilizers lamotrigine, lithium, valproate, carbamazepine, and oxcarbazepine. In general, if a patient has responded satisfactorily to a certain drug during the acute phase, the same treatment should be maintained during maintenance treatment. This was confirmed in two randomized controlled trials. This chapter summarizes the characteristics of the placebo-controlled randomized controlled trials for all the antipsychotics used for maintenance treatment of bipolar disorder.
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31

Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.

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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
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32

Ganança, Licínia, David A. Kahn, and Maria A. Oquendo. Mood Disorders. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0003.

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This chapter discusses the mood disorders. Major depressive disorder is characterized by neurovegetative changes, anhedonia, and suicidal ideation. Persistent depressive disorder is a milder form of depression, lasting for at least 2 years, with little or no remission during that time... Psychotic features can occur in both depressive and manic episodes. Premenstrual dysphoric disorder is diagnosed through use of a prospective daily symptom ratings log showing a cyclical pattern over at least 2 consecutive months. Patients with mood episodes with mixed features have a high risk of suicide. Some patients with bipolar disorder and major depressive disorder may develop catatonic features characterized by marked psychomotor disturbance. Selective serotonin reuptake inhibitors (SSRIs) are the usual first-line medication treatment for patients with major depressive disorder. For patients with bipolar disorder the mainstays of somatic therapy are lithium and the anticonvulsants valproate and carbamazepine.
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33

Kittel-Schneider, Sarah. The treatment of bipolar mixed states. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0005.

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Definition of mixed episodes has changed in the Diagnostic and Statistical Manual of Mental Disorders (5th edition) (DSM-5). A mixed feature specifier can be added not only to major depressive episodes and manic episodes in bipolar patients but also to hypomanic episodes in bipolar II patients and major depressive episode in major depressive disorder. Atypical antipsychotics seem to be effective in acute treatment as well as valproate and carbamazepine. Regarding prophylaxis of mixed states, monotherapy with valproate, olanzapine and quetiapine seems to prevent mixed episodes. Adjunctive therapy with valproate or lithium to quetiapine has also proven to be effective in prophylaxis of mixed episodes. In patients who suffer from pharmacotherapy-resistant mixed episodes electroconvulsive therapy can lead to response/remission. There is a lack of randomized controlled clinical trials investigating pharmacological and non-pharmacological treatments with focus on mixed states of bipolar patients, especially according to the DSM-5 definition.
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34

Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.
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35

Finnerup, Nanna Brix, and Troels Staehelin Jensen. Management issues in neuropathic pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0133.

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Neuropathic pain is a common complication to cancer, cancer treatment, HIV, and other conditions that may affect the somatosensory nervous system. Neuropathic pain may be present in up to 40% of cancer patients and may persist independently of the cancer and affect the quality of life in disease-free cancer survivors. Particular surgical treatment and chemotherapy may cause chronic persistent neuropathic pain in cancer survivors. The diagnosis of neuropathic pain can be challenging and requires documentation of a nervous system lesion and pain in areas of sensory changes. The pharmacological treatment may include tricyclic antidepressants, selective serotonin noradrenaline reuptake inhibitors (duloxetine or venlafaxine), calcium channel α2↓ agonists (gabapentin or pregabalin), and opioids. Topical lidocaine and capsaicin, NMDA antagonists, carbamazepine, oxcarbazepine, and cannabinoids may be indicated. Due to limited efficacy or intolerable side effects at maximal doses, combination therapy is often required and careful monitoring of effect and adverse reactions is important.
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