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Valproic acid

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Valproic acid chemical structure
Valproic acid

2-propylpentanoic acid
IUPAC name
CAS number
99-66-1
ATC code

N03AG01

PubChem
3121
DrugBank
APRD00256
Chemical formula {{{chemical_formula}}}
Molecular weight 144.211 g/mol
Bioavailability Rapid absorption
Metabolism Hepaticglucuronide conjugation 30–50%, mitochondrial β-oxidation over 40%
Elimination half-life 9–16 hours
Excretion Less than 3% excreted unchanged in urine.
Pregnancy category D—teratogenic
Legal status {{{legal_status}}}
Routes of administration Oral, intravenous

Valproic acid (VPA) is a chemical compound that has found clinical use as an anticonvulsant and mood-stabilizing drug, primarily in the treatment of epilepsy, bipolar disorder, and less commonly major depression. It is also used to treat migraine headaches and schizophrenia.

Related drugs include the sodium salts sodium valproate, used as an anticonvulsant, and a combined formulation, valproate semisodium, used as a mood stabilizer and additionally in the U.S. also as an anticonvulsant.

HistoryEdit

Valproic acid (by its official name 2-propylvaleric acid) was first synthesized in 1882 by Burton as an analogue of valeric acid, found naturally in the herb valerian.[1] A clear liquid fatty acid at room temperature, for many decades its only use was in laboratories as a "metabolically inert" solvent for organic compounds. In 1962, the French researcher Pierre Eymard serendipitously discovered the anticonvulsant properties of valproic acid while using it as a vehicle for a number of other compounds that were being screened for anti-seizure activity. He found that it prevented pentylenetetrazol-induced convulsions in rodents.[2] Since then it has also been used for migraine and bipolar disorder.[3]

PharmacologyEdit

Valproate is believed to affect the function of the neurotransmitter GABA (as a GABA transaminase inhibitor) in the human brain, making it an alternative to lithium salts in treatment of bipolar disorder.In addition to blocking transamination of GABA, Valproate is believed to reverse the transamination process to form more GABA. However, several other mechanisms of action in neuropsychiatric disorders have been proposed for valproic acid in recent years.[4].

Valproic acid also blocks the voltage-gated sodium channels and T-type Calcium channels.These mechanisms make Valproic Acid a Broad Spectrum Anticonvulsant drug.

Valproic acid is an inhibitor of the enzyme histone deacetylase 1 (HDAC1) hence it is a histone deacetylase inhibitor.

IndicationsEdit

As an anticonvulsant, valproic acid is used to control absence seizures, tonic-clonic seizures (grand mal), complex partial seizures, juvenile myoclonic epilepsy and the seizures associated with Lennox-Gastaut syndrome. It is also used in treatment of myoclonus. In some countries, parenteral (administered intravenously) preparations of valproate are used also as second-line treatment of status epilepticus, as an alternative to phenytoin. Valproate is one of the most common drugs used to treat post-traumatic epilepsy.[5]

According to Medical News Today, valproic acid can be used for the treatment of manic episodes associated with bipolar disorder, adjunctive therapy in multiple seizure types (including epilepsy), and prophylaxis of migraine headaches[6]. It is more recently being used to treat neuropathic pain, as a second line agent, particularly lancinating pain from A* fibres.

InvestigationalEdit

Histone deacetylase HDAC1 is needed for HIV to remain in infected cells. A study published in August 2005 found that three of four patients treated with valproic acid in addition to highly active antiretroviral therapy (HAART) showed a mean 75% reduction in latent HIV infection.[7] Subsequent trials, however, have found no long term benefits of valproic acid in HIV infection.[8]

According to the U.S. National Institutes of Health and others, valproic acid appears to have wide implications in the treatment of various cancers,[9] including multiple myeloma (bone marrow cancer),[10] glioma (an aggressive type of brain tumor),[11] and melanoma.[12] Valproic acid is cytotoxic to many different cancer types through its action as a histone deacetylase inhibitor. A phase I trial showed the maximum tolerated dose was 60 mg/kg.[13]

Another potential indication may be leukemia in juvenile patients. Studies conducted by several European centres are ongoing. Although it is too early to make a definitive statement, preliminary results are encouraging.[How to reference and link to summary or text]

Valproic acid gave encouraging results for breast cancer when used alongside a standard chemotherapy.[14]

In October, 2008 a research team at the University of British Columbia in Vancouver, Canada announced that in a study doses of valproic acid reversed the early stages of Alzheimer's disease in mice. Human trials are underway.

Valproic acid's function as an HDAC inhibitor has also led to its use in direct reprogramming in generation of induced pluripotent stem (iPS) cells, where it has been shown that addition of VPA allows for reprogramming of human fibroblasts to iPS cells without addition of genetic factors Klf4 and c-myc.

ContraindicationsEdit

Valproate is relatively contraindicated in pregnancy due to its teratogenicity; women who become pregnant while taking valproate should be counselled as to its risks, take high dose folic acid and be offered antenatal screening (alpha-fetoprotein and second trimester ultrasound scans).[15] It is a known folate antagonist, which can cause neural tube defects. Thus, folic acid supplements may alleviate the teratogenic problems. A recent study showed that children of mothers taking valproate during pregnancy are at risk for significantly lower IQs.[16][17] Exposure of the human embryo to valproic acid is also associated with risk of autism, and it is possible to duplicate features characteristic of autism by exposing rat embryos to valproic acid at the time of neural tube closure.[18] One study found that valproate exposure on embryonic day 11.5 led to significant local recurrent connectivity in the juvenile rat neocortex, consistent with the underconnectivity theory of autism.[19]

Valproate is contraindicated in overweight patients because it might cause weight gain.[How to reference and link to summary or text]

Preexisting hepatic (liver) and/or renal (kidney) damage or cancer, hepatitis, pancreatitis, end-stage AIDS HIV infection, bone marrow depression, urea cycle disorders, and coagulation hematological disorders are absolute contraindications.

Adverse effectsEdit

Common side effects are dyspepsia and/or weight gain. Less common are fatigue, peripheral edema, acne, dizziness, drowsiness, hair loss, headaches, nausea, sedation and tremors. Valproic acid also causes hyperammonemia, which can lead to brain damage.[20] Valproate levels within the normal range are capable of causing hyperammonemia and ensuing encephalopathy. There have been reports of brain encephalopathy developing without hyperammonemia or elevated valproate levels.[21]

Rarely, valproic acid can cause blood dyscrasia, impaired liver function, jaundice, thrombocytopenia, and prolonged coagulation times. In about 5% of pregnant users, valproic acid will cross the placenta and cause congenital anomalies. Due to these side effects, most doctors will ask for blood tests, initially as often as once a week and then once every 2 months. Temporary liver enzyme increase has been reported in 20% of cases during the first few months of taking the drug. Inflammation of the liver (hepatitis), the first symptom of which is jaundice, is found in rare cases.

Valproic acid may also cause acute hematological toxicities, especially in children, including rare reports of myelodysplasia and acute leukemia-like syndrome.[22][23]

There have also been reports of cognitive dysfunction, Parkinsonian symptoms[24], and even (reversible) pseudoatrophic brain changes[25] in long-term treatment with valproic acid.

InteractionsEdit

Valproic acid may interact with carbamazepine, as valproates inhibit microsomal epoxide hydrolase (mEH), the enzyme responsible for the breakdown of carbamazepine-10,11 epoxide (the main active metabolite of carbamazepine) into inactive metabolites.[26] By inhibiting mEH, valproic acid causes a buildup of the active metabolite, prolonging the effects of carbamazepine and delaying its excretion.

Valproic acid also decreases the clearance of amitriptyline and nortriptyline.[27]

Also, Valproic acid should not be used with the benzodiazopine clonazepam and aspirin to avoid adverse effects.

FormulationsEdit

Branded products include:
Depakene (Abbott Laboratories in U.S. & Canada)
Convulex (Pfizer in the UK and Byk Madaus in South Africa)
Stavzor (Noven Pharmaceuticals Inc.)
Depakine (Sanofi Aventis)
Epival (Abbott Laboratories U.S. & Canada)

ReferencesEdit

  1. Burton BS (1882). On the propyl derivatives and decomposition products of ethylacetoacetate. Am Chem J. 3:385-395.
  2. Meunier H, Carraz G, Meunier Y, Eymard P, Aimard M. (1963). Propriétés pharmacodynamiques de l’acide n-dipropylacetique. Therapie 18:435-438.
  3. Henry T.R. (2003). The History of Valproate in Clinical Neuroscience. Psychopharmacology bulletin 37 (Suppl 2):5-16
  4. Rosenberg G (2007). The mechanisms of action of valproate in neuropsychiatric disorders: can we see the forest for the trees?. Cellular and Molecular Life Sciences 64: 2090.
  5. Posner E, Lorenzo N (October 11, 2006). "Posttraumatic epilepsy". Emedicine.com. Retrieved on 2008-07-30.
  6. includeonly>"FDA Issues Approvable Letter For Stavzor Delayed Release Valproic Acid Capsules", 2007 MediLexicon International Ltd, 2007-10-25. Retrieved on 2007-10-29.
  7. Lehrman G, Hogue I, Palmer S, Jennings C, Spina C, Wiegand A, Landay A, Coombs R, Richman D, Mellors J, Coffin J, Bosch R, Margolis D (2005). Depletion of latent HIV-1 infection in vivo: a proof-of-concept study. Lancet 366 (9485): 549–55.
  8. Sagot-Lerolle N, Lamine A, Chaix ML, Boufassa F, Aboulker JP, Costagliola D, Goujard C, Paller C, Delfraissy JF, Lambotte O; ANRS EP39 study (2008). Prolonged valproic acid treatment does not reduce the size of latent HIV reservoir. AIDS 22 (10): 1125–29.
  9. Isenberg JS, Jia Y, Field L, Ridnour LA, Sparatore A, Del Soldato P, Sowers AL, Yeh GC, Moody TW, Wink DA, Ramchandran R, Roberts DD (2007). Modulation of angiogenesis by dithiolethione-modified NSAIDs and valproic acid.. British Journal of Pharmacology Mar 12.
  10. Schwartz C, Palissot V, Aouali N, Wack S, Brons NH, Leners B, Bosseler M, Berchem G (2007). Valproic acid induces non-apoptotic cell death mechanisms in multiple myeloma cell lines.. International Journal of Oncology Mar (30): 573–82.
  11. A.M. Admirant, J. A. Hendricks, P.C. De Witt Hamer, S. Leenstra, W.P. Vandertop, C.J.F. van Noorden, and J.P. Medema (2006). Valproic Acid is toxic to malignant glioma cells and increases sensitivity to irradiation and chemotherapy. Abstracts for the Seventh Congress of the European Association for Neuro-Oncology (EANO) Sept 14-17: 334.
  12. Valentini A, Gravina P, Federici G, Bernardini S. (2007). Valproic Acid Induces Apoptosis, p(16INK4A) Upregulation and Sensitization to Chemotherapy in Human Melanoma Cells. Cancer Biology & Therapy Feb 5 (6).
  13. http://meeting.ascopubs.org/cgi/content/abstract/22/14_suppl/3169
  14. http://www.asco.org/ASCO/Abstracts+&+Virtual+Meeting/Abstracts?&vmview=abst_detail_view&confID=47&abstractID=32900
  15. British National Formulary (March 2003) 45
  16. Cassels, Caroline NEAD: In Utero Exposure To Valproate Linked to Poor Cognitive Outcomes in Kids. Medscape. URL accessed on 2007-05-23.
  17. Meador KJ, Baker GA, Finnell RH, et al (2006). In utero antiepileptic drug exposure: fetal death and malformations. Neurology 67 (3): 407–12.
  18. Arndt TL, Stodgell CJ, Rodier PM (2005). The teratology of autism. Int J Dev Neurosci 23 (2–3): 189–99.
  19. Rinaldi T, Silberberg G, Markram H (2007). Hyperconnectivity of local neocortical microcircuitry induced by prenatal exposure to valproic acid. Cereb Cortex 18: 763.
  20. Valproate-associated Hyperammonemic Encephalopathy - Wadzinski et al. 20 (5): 499 - The Journal of the American Board of Family Medicine
  21. Thieme-connect - Abstract
  22. Williams DC Jr, Massey GV, Russell EC, Riley RS, Ben-Ezra J. (2007). Translocation positive acute myeloid leukemia associated with valproic acid therapy. Pediatric Blood and Cancer Mar 29: 641.
  23. Coyle TE, Bair AK, Stein C, Vajpayee N, Mehdi S, Wright J. (2005). Acute leukemia associated with valproic acid treatment: a novel mechanism for leukemogenesis?. Pediatric Blood and Cancer Apr (78): 256–60.
  24. Ricard C, Martin K, Tournier M, Bégaud B, Verdoux H (2005). [A case of Parkinsonian syndrome, cognitive impairment and hyperammonemia induced by divalproate sodium prescribed for bipolar disorder]. L'Encéphale 31 (1 Pt 1): 98–101.
  25. McLachlan RS (1987). Pseudoatrophy of the brain with valproic acid monotherapy. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 14 (3): 294–6.
  26. Gonzalez, Frank J.; Robert H. Tukey (2006). "Drug Metabolism" Laurence Brunton, John Lazo, Keith Parker (eds.) Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11th, 79, New York: McGraw-Hill.
  27. (2007). Depakene side effects (Valproic Acid) and drug interactions. RxList.com. URL accessed on 2007-06-07.

Further readingEdit

Key textsEdit

BooksEdit

  • Bowden, C. L. (2004). Valproate. New York, NY: American Psychoanalytic Association.
  • Bowden, C. L., & Singh, V. (2006). Valproate: Clinical Pharmacological Profile. Hoboken, NJ: John Wiley & Sons Inc.
  • West, S. A., McElroy, S. L., & Keck, P. E., Jr. (1998). Valproate. Washington, DC: American Psychiatric Association.

PapersEdit

  • Abbas, A., & Styra, R. (1994). Valproate prophylaxis against steroid induced psychosis: The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie Vol 39(3) Apr 1994, 188-189.
  • Adewuya, E. C., Zinser, W., & Thomas, C. (2008). Trichotillomania: A case of response to valproic acid: Journal of Child and Adolescent Psychopharmacology Vol 18(5) Oct 2008, 533-536.
  • Agmo, A., Medrano, A., Garrido, N., & Alonso, P. (1997). GABAergic drugs inhibit amphetamine-induced distractibility in the rat: Pharmacology, Biochemistry and Behavior Vol 58(1) Sep 1997, 119-126.
  • Akdeniz, F. (2001). The effects of valproate on female reproductive endocrine function: Turk Psikiyatri Dergisi Vol 12(4) 2001, 301-307.
  • Akdeniz, F., Taneli, F., Noyan, A., Yuncu, Z., & Vahip, S. (2003). Valproate-associated reproductive and metabolic abnormalities: Are epileptic women at greater risk than bipolar women? : Progress in Neuro-Psychopharmacology & Biological Psychiatry Vol 27(1) Feb 2003, 115-121.
  • Akimoto, T., Kusumi, I., Suzuki, K., Masui, T., & Koyama, T. (2007). Effects of valproate on serotonin-induced intracellular calcium mobilization in human platelets: Journal of Psychiatry & Neuroscience Vol 32(1) Jan 2007, 17-22.
  • Albanese, M. J., Clodfelter, R. C., Jr., & Khantzian, E. J. (2000). Divalproex sodium in substance abusers with mood disorder: Journal of Clinical Psychiatry Vol 61(12) Dec 2000, 916-921.
  • Alcantara, A. C., Perez, M. S., del Campo, M. D., & Irastorza, G. R. (2005). Eosinophilic la efusion pleural secundaria al tratamiento con el acido de valproic: Actas Espanolas de Psiquiatria Vol 33(6) Nov-Dec 2005, 401-402.
  • Aldenkamp, A., Vigevano, F., Arzimanoglou, A., & Covanis, A. (2006). Role of valproate across the ages. Treatment of epilepsy in children: Acta Neurologica Scandinavica Vol 114(Suppl 184) Aug 2006, 1-13.
  • Ali, S., Pearlman, R. L., Upadhyay, A., & Patel, P. (2006). Neuroleptic Malignant Syndrome With Aripiprazole and Lithium: A Case Report: Journal of Clinical Psychopharmacology Vol 26(4) Aug 2006, 434-436.
  • Aliyev, N. A., & Aliyev, Z. N. (2008). Valproate (depakine-chrono) in the acute treatment of outpatients with generalized anxiety disorder without psychiatric comorbidity: Randomized, double-blind placebo-controlled study: European Psychiatry Vol 23(2) Mar 2008, 109-114.
  • Allen, M. H., Hirschfeld, R. M., Wozniak, P. J., Baker, J. D., & Bowden, C. L. (2006). Linear Relationship of Valproate Serum Concentration to Response and Optimal Serum Levels for Acute Mania: American Journal of Psychiatry Vol 163(2) Feb 2006, 272-275.
  • Altamura, A. C., Russo, M., Vismara, S., & Mundo, E. (2004). Comparative Evaluation of Olanzapine Efficacy in the Maintenance Treatment of Bipolar Disorder: Journal of Clinical Psychopharmacology Vol 24(4) Aug 2004, 454-456.
  • Alves, N. D., de Castro-Costa, C. M., de Carvalho, A. M., Santos, F. J. C., & Silveira, D. G. (1999). Possible analgesic effect of vigabatrin in animal experimental chronic neuropathic pain: Arquivos de Neuro-Psiquiatria Vol 57(4) Dec 1999, 916-920.
  • Ambrosini, P. J., & Sheikh, R. M. (1998). Increased plasma valproate concentrations when coadministered with guanfacine: Journal of Child and Adolescent Psychopharmacology Vol 8(2) 1998, 143-147.
  • Ananth, J. (1999). Is olanzapine a mood stabilizer? : The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie Vol 44(9) Nov 1999, 927-928.
  • Anastasov, V. F., Stoev, V., Prosev, I., & Hristovska, S. (2004). Plasma level of valproic acid in treatment of severe cases of schizoaffective psychoses and rapid cycling bipolar disorders: Psychiatria Danubina Vol 16(4) Dec 2004, 325-326.
  • Angelini, G., Berra, L., Astegiano, G., & Sabbatini, F. (1995). Sexual dysfunctions and epilepsy in males: Minerva Psichiatrica Vol 36(4) Dec 1995, 209-211.
  • Applebaum, J., Bersudsky, Y., & Klein, E. (2007). Rapid tryptophan depletion as a treatment for acute mania: A double-blind, pilot-controlled study: Bipolar Disorders Vol 9(8) Dec 2007, 884-887.
  • Arban, R., Maraia, G., Brackenborough, K., Winyard, L., Wilson, A., Gerrard, P., et al. (2005). Evaluation of the effects of lamotrigine, valproate and carbamazepine in a rodent model of mania: Behavioural Brain Research Vol 158(1) Mar 2005, 123-132.
  • Armour, D. (2000). Prescribing and monitoring of valproate: Psychiatric Bulletin Vol 24(10) Oct 2000, 395.
  • Arndt, C. F., Salle, M., Derambure, P. H., Defoort-Dhellemmes, S., & Hache, J.-C. (2002). The effect on vision of associated treatments in patients taking vigabatrin: Carbamazepine versus valproate: Epilepsia Vol 43(8) Aug 2002, 812-817.
  • Arndt, T. L., Stodgell, C. J., & Rodier, P. M. (2005). The teratology of autism: International Journal of Developmental Neuroscience Vol 23(2-3) Apr-May 2005, 189-199.
  • Atmaca, M., Yildirim, H., Ozdemir, H., Ogur, E., & Tezcan, E. (2007). Hippocampal superscript 1H MRS in patients with bipolar disorder taking valproate versus valproate plus quetiapine: Psychological Medicine Vol 37(1) Jan 2007, 121-129.
  • Aubry, J.-M., Ragama-Pardos, E., Favre, S., Menzinger, M., Muscionico, M., Sanchez, S., et al. (2003). Efficacy and safety of olanzapine plus valproate in the treatment of acute mania: An open study: International Journal of Psychiatry in Clinical Practice Vol 7(2) Jun 2003, 131-134.
  • Aycicek, A., & lscan, A. (2007). The effects of carbamazepine, valproic acid and phenobarbital on the oxidative and antioxidative balance in epileptic children: European Neurology Vol 57(2) 2007, 65-69.
  • Aydin, S., & Dag, E. (2008). Does ghrelin really increase in epileptic children treated with valproate? : Journal of Child Neurology Vol 23(9) Sep 2008, 1084.
  • Azorin, J. M., & Findling, R. L. (2007). Valproate use in children and adolescents with bipolar disorder: CNS Drugs Vol 21(12) Dec 2007, 1019-1033.
  • Baetz, M., & Bowen, R. C. (1998). Efficacy of divalproex sodium in patients with panic disorder and mood instability who have not responded to conventional therapy: The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie Vol 43(1) Feb 1998, 73-77.
  • Bajwa, Z. H., Sami, N., & Wootton, J. (1999). Successful use of divalproex sodium in the abortive treatment of a severe migraine attack: Headache Quarterly Vol 10(3) 1999, 225-227.
  • Baker, C. B., Woods, S. W., & Sernyak, M. J. (1997). Cost-effectiveness of divalproex versus lithium: Journal of Clinical Psychiatry Vol 58(8) Aug 1997, 363.
  • Baker, R. W., Brown, E., Akisk Al, H. S., Calabrese, J. R., Ketter, T. A., Schuh, L. M., et al. (2004). Efficacy of olanzapine combined with valproate or lithium in the treatment of dysphoric mania: British Journal of Psychiatry Vol 185(6) Dec 2004, 472-478.
  • Baldessarini, R. J., Centorrino, F., Flood, J. G., Frankenburg, F. R., & et al. (1995). "Serum concentrations of clozapine and its major metabolites: Effects of cotreatment with fluoxetine or valproate": Reply: American Journal of Psychiatry Vol 152(3) Mar 1995, 473-474.
  • Baldessarini, R. J., Tohen, M., & Tondo, L. (2000). Maintenance treatment in bipolar disorder: Archives of General Psychiatry Vol 57(5) May 2000, 490-492.
  • Baldessarini, R. J., & Tondo, L. (2003). Suicide risk and treatments for patients with bipolar disorder: JAMA: Journal of the American Medical Association Vol 290(11) Sep 2003, 1517-1519.
  • Balen, R. M., & Procyshyn, R. M. (1999). Valproic acid for seizure prophylaxis during clozapine therapy: Where's the evidence? : International Journal of Psychiatry in Clinical Practice Vol 3(4) Dec 1999, 249-251.
  • Barkai, G., Goshen, E., Zwas, S. T., Dolberg, O. T., Pick, C. G., Bonne, O., et al. (2004). Acetazolamide-enhanced neuroSPECT scan reveals functional impairment after minimal traumatic brain injury not otherwise discernible: Psychiatry Research: Neuroimaging Vol 132(3) Dec 2004, 279-283.
  • Barnhill, J., & Carlos, A. (1997). Phenobarbital-induced disinhibition in the developmentally disabled: Case report: Journal of Clinical Psychopharmacology Vol 17(3) Jun 1997, 229-230.
  • Basan, A., Kissling, W., & Leucht, S. (2004). Valproate as an adjunct to antipsychotics for schizophrenia: a systematic review of randomized trials: Schizophrenia Research Vol 70(1) Sep 2004, 33-37.
  • Bates, E., Florit, G., & Hussain, M. (1997). Mood stabilizers and drug interactions: Journal of Clinical Psychiatry Monograph Series Vol 15(4) Oct 1997, 31-34.
  • Bauer, J. (2008). Encephalopathy induced by levetiracetam added to valproate: Acta Neurologica Scandinavica Vol 117(5) May 2008, 374-376.
  • Bauer, M. S. (2005). Fatal Hepatic Failure and Valproate: American Journal of Psychiatry Vol 162(1) Jan 2005, 192.
  • Baumann, R. J., Fakhoury, T. A., Kustra, R. P., Vuong, A., Hammer, A. E., & Messenheimer, J. A. (2007). Conversion to lamotrigine monotherapy from valproate monotherapy in older adolescent patients with epilepsy: Current Medical Research and Opinion Vol 23(10) Oct 2007, 2461-2465.
  • Bayer, A. U., Thiel, H. J., Zrenner, E., Dichgans, J., & et al. (1997). Color vision tests for early detection of antiepileptic drug toxicity: Neurology Vol 48(5) May 1997, 1394-1397.
  • Bazinet, R. P., Weis, M. T., Rapoport, S. I., & Rosenberger, T. A. (2006). Valproic acid selectively inhibits conversion of arachidonic acid to arachidonoyl-CoA by brain microsomal long-chain fatty acyl-CoA synthetases: relevance to bipolar disorder: Psychopharmacology Vol 184(1) Jan 2006, 122-129.
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  • Beenen, L. F. M., Lindeboom, J., Kasteleijn-Nolst Trenite, D. G. A., Heimans, J. J., Snoek, F. J., Touw, D. J., et al. (1999). Comparative double blind clinical trial of phenytoin and sodium valproate as anticonvulsant prophylaxis after craniotomy: efficacy, tolerability, and cognitive effects: Journal of Neurology, Neurosurgery & Psychiatry Vol 67(4) Oct 1999, 474-480.
  • Bell, E. C., Willson, M. C., Wilman, A. H., Dave, S., & Silverstone, P. H. (2005). Differential effects of chronic lithium and valproate on brain activation in healthy volunteers: Human Psychopharmacology: Clinical and Experimental Vol 20(6) Aug 2005, 415-424.
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  • Benjelloun, G., Blandin, K., & Fossati, P. (2004). Valpromide, Valproic acid and removal of hail intestine in the treatment of a chronic depression: A case report: L'Encephale Vol 30(4) Jul-Aug 2004, 400-403.
  • Ben-Menachem, E., Schmitz, B., Tomson, T., & Vajda, F. (2006). Role of valproate across the ages. Treatment of epilepsy in adults: Acta Neurologica Scandinavica Vol 114(Suppl 184) Aug 2006, 14-27.
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DissertationsEdit

  • Gavin, J. A. L. (2008). Neurobehavioral outcomes in infants prenatally exposed to valproic acid. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Grimes, C. A. (2001). Effects of mood stabilizers on transcription factors. Dissertation Abstracts International: Section B: The Sciences and Engineering.
  • Watterson, J. M. (2000). In vitro studies on a putative molecular mechanism of action of valproic acid in treatment of bipolar disorder. Dissertation Abstracts International: Section B: The Sciences and Engineering.


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