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Beyond Lithium in the Treatment of Bipolar Illness Robert M. Post, M.D., Mark A. Frye, M.D., Kirk D. Denicoff, M.D., Gabriele S. Leverich, L.C.S.W., Tim A. Kimbrell, M.D., and Robert T. Dunn, M.D. Dramatic changes have recently occurred in the availability lamotrigine, gabapentin, and topiramate have unique of treatment options for bipolar illness. Second generation mechanisms of action and deserve further systematic study, mood stabilizing anticonvulsants carbamazepine and as does the potential role for nonconvulsive brain valproate are now widely used as alternatives or adjuncts to stimulation with repeated transcranial magnetic lithium. High potency benzodiazepines are also used as stimulation (rTMS). These and a host of other potential alternatives to typical neuroleptics, and now atypical treatment options now require a new generation of clinical neuroleptics are demonstrating efficacy and better side- trials to help identify clinical and biological markers of effects profiles than the typicals. Thyroid augmentation response and optimal use alone and in complex combination strategies and dihydropyridine L-type calcium channel therapeutic regimens. [Neuropsychopharmacology blockers require further clinical trials to define their role. 19:206–219, 1998] Published by Elsevier Science Inc. Putative third generation mood stabilizing anticonvulsants KEY WORDS: Carbamazepine; Valproate; Calcium channel al. 1989; O’Connell et al. 1991; Denicoff et al. 1997); a blockers; Lamotrigine; Gabapentin; rTMS history of co-morbid substance abuse; and those pa- tients with a history of head trauma or other such medi- There is increasing recognition of the inadequacy of cal co-morbidities as multiple sclerosis, etc. “lithium treatment” in bipolar illness, even with ad- In addition, it is recognized that patients with initial junctive antidepressants and neuroleptics (Maj et al. excellent responses to lithium can begin to develop 1989; Aagaard and Vestergaard 1990; O’Connell et al. breakthrough episodes in subsequent extended years of 1991; Vestergaard 1992; Gitlin et al. 1995). Some bipolar follow-up (Maj et al. 1989; Post et al. 1992). In our series patient subtypes are particularly prone to lithium non- of 66 lithium-refractory patients, 23 (34.9%) seem to responsiveness; among these are patients with dyspho- have developed their lithium-refractoriness over more ric mania and rapid cycling; a negative family history prolonged periods of follow-up, in a pattern resembling for bipolar illness in first-degree relatives; the episode tolerance. sequence pattern of depression-mania-well interval Another recently described route to refractoriness (i.e., the D-M-I pattern as opposed to the M-D-I pat- has been found in patients who were excellent respond- tern); more than three episodes prior to the initiation of ers to lithium, but then discontinued treatment (on the prophylaxis (Sarantidis and Waters 1981; Gelenberg et basis of either noncompliance or physician acquies- cence), experienced a relapse, and then failed to re- From the Biological Psychiatry Branch, National Institute of Men- respond once lithium was reinstituted (Post et al. 1992, tal Health, Bethesda, Maryland, USA. 1993; Koukopoulos et al. 1995). This type of lithium dis- Address correspondence to: Robert M. Post, M.D., Chief Biologi- continuation-induced refractoriness can be quite malig- cal Psychiatry Branch, NIMH, Bldg. 10, Room 3N212, 10 Center Drive MSC 1272, Bethesda, Maryland 20892-1272, USA. nant, with patients failing to re-respond, even when Received February 23, 1998; accepted February 23, 1998. lithium is augmented with a variety of the other alter- NEUROPSYCHOPHARMACOLOGY 1998–VOL. 19, NO. 3 Published by Elsevier Science Inc. 0893-133X/98/$19.00 655 Avenue of the Americas, New York, NY 10010 PII S0893-133X(98)00020-7 N EUROPSYCHOPHARMACOLOGY Table 1. Controlled Studies of Carbamazepine (CBZ) and Oxcarbazepine (OXCBZ) in Acute Mania Doses (mg/day) Outcome a Study Diagnosis Design [blood level] Other Drugs Duration Measures Results n Ballenger and 19 CBZ Manic D-Bl (B-A-B-A) 600–2,000-mg CBZ None 11–56 Days Bunney- 12/19 (63%) Improved time course similar to m Post 1978; 19 Placebo randomized [8–12 g/ml] Hamburg neuroleptics; frequent relapses on placebo Post et al. 1984a, BPRS substitution 1987 Okuma et al. 1979 30 CBZ Manic D-Bl. vs. CPZ 300–900-mg CBZ Bedtime hypnotics 3–5 Weeks CPRG 21/30 (70%) Improved on CBZ m 25 CPZ randomized [2.7–11.7 g/ml] 15/25 (60%) Improved on CPZ (moderate to 5 6 [mean 7.2 3.4] marked) 150–450-mg CPZ Fewer side effects on CBZ m 1998 [2.6–311.4 g/ml] Slightly faster onset with CBZ Grossi et al. 1984 15 CBZ Manic D-Bl. vs. CPZ 200-1,200-mg CBZ Bedtime hypnotics 3 Weeks MSRS BMS 10/15 (67%) improved on CBZ – 6 VOL 17 CPZ randomized [mean 655.5 295.5] 10/17 (59%) improved on CPZ (moderate to 200–800 mg CPZ marked) [mean 362.5 6 166.83] Fewer side effects with CBZ than CPZ . Slightly faster onset with CBZ 19 , Klein et al. 1984 23 CBZ Manic/ D-Bl. vs. 600–1,200-mg CBZ Halo 5 Weeks BPRS GCI 13/23 (57%) BPRS improvement CBZ1halo NO m 1 20 Placebo excited placebo addition to halo [8–12 g/ml] 15–45 11/20 (55%) BPRS improvmeent plac halo . S/SA randomized mg all Improvement in GCI in both groups 3 patients Muller and Stoll 10 OXCBZ Mania D-Bl. vs. halo 900–1,200 mg OXCBZ Halo and hypnotics 2 Weeks BRMS BRMS scores decreased in both groups; onset 1984 10 Halo randomized 15–20 mg halo faster with OXCBZ Goncalves and Stoll 6 CBZ Manic SA D-Bl. vs. 200–1,200 mg CBZ Halo and hypnotics 3 Weeks MS-M 6/6 CBZ better than placebo (p , .01) 1985 6 Placebo placebo randomized Emrich et al. 1985 7 OXCBZ Manic D-Bl. (B-A-B) 1,800–2,100 mg (max. None Variable IMPS 6/7 (86%) Improved with OXCBZ (.25% 5 placebo psycho- dosage range) Improvement on IMPS) sis OXCBZ Lenzi et al. 1986 11 CBZ Excitation D-Bl. vs. Li 400–1,600 mg CBZ CPZ all patients 19 Days BPRS CGI Significant improvement with CBZ and Li on 11 Li psycho- randomized [7–12 mg/ml] average CGI and BPRS sis 300–900 mg Li CBZ group required less CPZ [0.6–1.2 mEq/l] CBZ less paranoia and EPS Stoll et al. 1986 14 CBZ Manic Randomized 600–1,200 mg CBZ Neuroleptics 3 Weeks MS-M 12/14 (86%) Improved on CBZ 18 Halo vs. halo 5–30 mg halo Hypnotics 12/18 (67%) Improved on halo (good to very good) Desai et al. 1987 5 CBZ Manic D-Bl. vs. pla- 400 mg fixed dose Li all patients 4 Weeks BRMS GMS CBZ 1 Li better BRMS and GMS than Li alone Beyond LithiuminBipolarIllness 5 Placebo cebo addi- CBZ [0.5–1.7 mEq/l] (p , .05) tion to Li randomized Lerer et al. 1987 14 CBZ Manic D-Bl. vs. Li 600–2,600-mg CBZ Chloral hydrate 4 Weeks CGI BPRS 4/14 (29%) Improved CGI score on CBZ (p , 14 Li randomized [3.2–14 mg/ml] barbiturates MSRS .05) 900–3,900-mg Li H.S. 11/14 (79%) Improved CGI score on Li [0.2–2.0 mEq/l) BPRS and MSRS scores improved with both CBZ and Li, nonsignificantly Lusznat et al. 1988 22 CBZ Manic/ D-Bl. vs. Li 200-mg CBZ until serum CPZ, halo, 6 Weeks BRMS No significant differences 22 Li hypo- randomized lvl 6–12 mg/ml neuroleptics manic 400-mg Li until serum lvl 0.6–1.4 mmol/l Okuma et al. 1988 103 CBZ Manic D-Bl. vs. Antipsychotics Global 50% Global improvement rate on CBZ 98 Placebo placebo improve- 30% Global improvement rate on placebo ment rate (moderate to marked) 207 (continued) 208 R.M. Postetal. N Table 1. (continued) Doses (mg/day) Outcome Study na Diagnosis Design [blood level] Other Drugs Duration Measures Results Brown et al. 1989 8 CBZ Manic D-Bl. vs. halo 400–1,600 mg CBZ CPZ 4 Weeks YMS 6/8 (75%) Marked improvement on CBZ 9 Halo randomized 20–80 mg halo PMS 3/9 (33%) Marked improvement on halo CBZ slower onset, higher completion rate (75%) vs. 22%), fewer EPS Moller et al. 1989 11 CBZ Manic or D-Bl. vs. 600 mg CBZ Halo 24 mg all 3 Weeks BRMS Both groups highly significant antimanic effect 9 Placebo SA placebo patients Levo- BPRS on all scales mepromazine MS-M No significant difference between groups CBZ group needed less levomepromazine Emrich 1990 19 OXCBZ Manic D-Bl. vs. halo 2,400-mg mean dose 15 Days BRMS Both groups significantly lowered BRMS score 19 Halo OXCBZ Side effects 3 1/2 times greater in halo group 42-mg mean dose halo Emrich 1990 28 OXCBZ Manic D-Bl. vs. Li 1,400-mg mean dose 15 Days BPRS Both groups significantly lowered BRMS score 24 Li OXCBZ Side effects slightly higher in OXCBZ group Okuma et al. 1990 50 CBZ Manic D-Bl. vs. Li 400–1,200-mg CBZ Neuroleptics 4 Weeks CPRG 31/50 (62%) Improved on CBZ 5 m 51 Li [mean 7.3 g/ml] Bedtime hypnotics 30/51 (59%) Improved on Li 400–1,200-mg Li No significant difference between groups 5 [mean 0.46 mEq/l] CBZ onset earlier, greater EPS Small et al. 1991 24 CBZ Manic D-Bl. vs. Li 700–1036-mg CBZ Hypnotics 6–8 Weeks SDMS-D&M 8/24 (33%) Improved on CBZ 24 Li randomized [30–37 mmol/l] YMS 8/24 (33%) Improved on Li 1,035–1,278 mg Li BPRS No significant difference between groups after EUROPSYCHOPHARMACOLOGY [0.6–0.9 mmol/l] CGI 8 weeks Total of all 19 355 pts.
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  • Pharmacokinetic and Pharmacodynamic Interactions Between Antiepileptics and Antidepressants Domenico Italiano University of Messina, Italy

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    University of Kentucky UKnowledge Psychiatry Faculty Publications Psychiatry 11-2014 Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants Domenico Italiano University of Messina, Italy Edoardo Spina University of Messina, Italy Jose de Leon University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits oy u. Follow this and additional works at: https://uknowledge.uky.edu/psychiatry_facpub Part of the Psychiatry and Psychology Commons Repository Citation Italiano, Domenico; Spina, Edoardo; and de Leon, Jose, "Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants" (2014). Psychiatry Faculty Publications. 40. https://uknowledge.uky.edu/psychiatry_facpub/40 This Article is brought to you for free and open access by the Psychiatry at UKnowledge. It has been accepted for inclusion in Psychiatry Faculty Publications by an authorized administrator of UKnowledge. For more information, please contact [email protected]. Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants Notes/Citation Information Published in Expert Opinion on Drug Metabolism & Toxicology, v. 10, Issue 11, p. 1457-1489. © 2014 Taylor & Francis Group This is an Accepted Manuscript of an article published by Taylor & Francis Group in Expert Opinion on Drug Metabolism & Toxicology in Nov. 2014, available online: http://www.tandfonline.com/10.1517/ 17425255.2014.956081 Digital Object Identifier (DOI) http://dx.doi.org/10.1517/17425255.2014.956081 This article is available at UKnowledge: https://uknowledge.uky.edu/psychiatry_facpub/40 1 This is an Accepted Manuscript of an article published by Taylor & Francis Group in Expert Opinion on Drug Metabolism & Toxicology in Nov.