Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders

Terence A. Ketter, Tim A. Kimbrell, Mark S. George, Mark W. Willis, Brenda E. Benson, Aimee Danielson, Mark A Frye, Peter Herscovitch, Robert M. Post

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

Background: Positron emission tomography (PET) studies have reported baseline (medication free) differences between mood disorder patients and healthy control subjects, but relatively little is known about relationships between baseline PET scans and treatment responses. Carbamazepine (CBZ) and to a more limited extent nimodipine (NIMO) seem useful in mood disorders. We explored whether baseline regional cerebral glucose metabolism (rCMRglu) could discriminate CBZ and NIMO responders from nonresponders and healthy control subjects. Methods: In refractory mood disorder patients, we examined relationships between responses to these drugs, assessed by Clinical Global Impression-Improvement scores, and baseline rCMRglu, determined with fluorine-18 deoxyglucose and PET. Results: CBZ responders had baseline left insular hypermetabolism compared to healthy control subjects and nonresponders, whereas nonresponders had widespread (including left insular) hypometabolism. Degree of CBZ response correlated with baseline paralimbic (including insula) and prefrontal hypermetabolism. In responders but not nonresponders, CBZ decreased widespread metabolism, with the degree of decrease in left insula correlating with response. In contrast, NIMO responders but not nonresponders had baseline widespread (including left insular) hypometabolism. Left prefrontal and left insular baseline hypometabolism, but not metabolic changes with treatment correlated with degree of NIMO response. Conclusions: These data suggest that baseline anterior paralimbic and prefrontal hypermetabolism may be associated with CBZ response, and hypometabolism with NIMO response. Based on these preliminary data, further exploration of relationships between baseline PET scans and treatment responses is indicated.

Original languageEnglish (US)
Pages (from-to)1364-1374
Number of pages11
JournalBiological Psychiatry
Volume46
Issue number10
DOIs
StatePublished - Nov 15 1999
Externally publishedYes

Fingerprint

Nimodipine
Carbamazepine
Mood Disorders
Positron-Emission Tomography
Healthy Volunteers
Fluorine
Deoxyglucose
Therapeutics
Glucose
Pharmaceutical Preparations

Keywords

  • Carbamazepine
  • Cerebral
  • Metabolism
  • Mood disorders
  • Nimodipine
  • PET

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

Ketter, T. A., Kimbrell, T. A., George, M. S., Willis, M. W., Benson, B. E., Danielson, A., ... Post, R. M. (1999). Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders. Biological Psychiatry, 46(10), 1364-1374. https://doi.org/10.1016/S0006-3223(99)00210-3

Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders. / Ketter, Terence A.; Kimbrell, Tim A.; George, Mark S.; Willis, Mark W.; Benson, Brenda E.; Danielson, Aimee; Frye, Mark A; Herscovitch, Peter; Post, Robert M.

In: Biological Psychiatry, Vol. 46, No. 10, 15.11.1999, p. 1364-1374.

Research output: Contribution to journalArticle

Ketter, TA, Kimbrell, TA, George, MS, Willis, MW, Benson, BE, Danielson, A, Frye, MA, Herscovitch, P & Post, RM 1999, 'Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders', Biological Psychiatry, vol. 46, no. 10, pp. 1364-1374. https://doi.org/10.1016/S0006-3223(99)00210-3
Ketter, Terence A. ; Kimbrell, Tim A. ; George, Mark S. ; Willis, Mark W. ; Benson, Brenda E. ; Danielson, Aimee ; Frye, Mark A ; Herscovitch, Peter ; Post, Robert M. / Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders. In: Biological Psychiatry. 1999 ; Vol. 46, No. 10. pp. 1364-1374.
@article{66cdd8127a304b389597ade08767dab9,
title = "Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders",
abstract = "Background: Positron emission tomography (PET) studies have reported baseline (medication free) differences between mood disorder patients and healthy control subjects, but relatively little is known about relationships between baseline PET scans and treatment responses. Carbamazepine (CBZ) and to a more limited extent nimodipine (NIMO) seem useful in mood disorders. We explored whether baseline regional cerebral glucose metabolism (rCMRglu) could discriminate CBZ and NIMO responders from nonresponders and healthy control subjects. Methods: In refractory mood disorder patients, we examined relationships between responses to these drugs, assessed by Clinical Global Impression-Improvement scores, and baseline rCMRglu, determined with fluorine-18 deoxyglucose and PET. Results: CBZ responders had baseline left insular hypermetabolism compared to healthy control subjects and nonresponders, whereas nonresponders had widespread (including left insular) hypometabolism. Degree of CBZ response correlated with baseline paralimbic (including insula) and prefrontal hypermetabolism. In responders but not nonresponders, CBZ decreased widespread metabolism, with the degree of decrease in left insula correlating with response. In contrast, NIMO responders but not nonresponders had baseline widespread (including left insular) hypometabolism. Left prefrontal and left insular baseline hypometabolism, but not metabolic changes with treatment correlated with degree of NIMO response. Conclusions: These data suggest that baseline anterior paralimbic and prefrontal hypermetabolism may be associated with CBZ response, and hypometabolism with NIMO response. Based on these preliminary data, further exploration of relationships between baseline PET scans and treatment responses is indicated.",
keywords = "Carbamazepine, Cerebral, Metabolism, Mood disorders, Nimodipine, PET",
author = "Ketter, {Terence A.} and Kimbrell, {Tim A.} and George, {Mark S.} and Willis, {Mark W.} and Benson, {Brenda E.} and Aimee Danielson and Frye, {Mark A} and Peter Herscovitch and Post, {Robert M.}",
year = "1999",
month = "11",
day = "15",
doi = "10.1016/S0006-3223(99)00210-3",
language = "English (US)",
volume = "46",
pages = "1364--1374",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",
number = "10",

}

TY - JOUR

T1 - Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders

AU - Ketter, Terence A.

AU - Kimbrell, Tim A.

AU - George, Mark S.

AU - Willis, Mark W.

AU - Benson, Brenda E.

AU - Danielson, Aimee

AU - Frye, Mark A

AU - Herscovitch, Peter

AU - Post, Robert M.

PY - 1999/11/15

Y1 - 1999/11/15

N2 - Background: Positron emission tomography (PET) studies have reported baseline (medication free) differences between mood disorder patients and healthy control subjects, but relatively little is known about relationships between baseline PET scans and treatment responses. Carbamazepine (CBZ) and to a more limited extent nimodipine (NIMO) seem useful in mood disorders. We explored whether baseline regional cerebral glucose metabolism (rCMRglu) could discriminate CBZ and NIMO responders from nonresponders and healthy control subjects. Methods: In refractory mood disorder patients, we examined relationships between responses to these drugs, assessed by Clinical Global Impression-Improvement scores, and baseline rCMRglu, determined with fluorine-18 deoxyglucose and PET. Results: CBZ responders had baseline left insular hypermetabolism compared to healthy control subjects and nonresponders, whereas nonresponders had widespread (including left insular) hypometabolism. Degree of CBZ response correlated with baseline paralimbic (including insula) and prefrontal hypermetabolism. In responders but not nonresponders, CBZ decreased widespread metabolism, with the degree of decrease in left insula correlating with response. In contrast, NIMO responders but not nonresponders had baseline widespread (including left insular) hypometabolism. Left prefrontal and left insular baseline hypometabolism, but not metabolic changes with treatment correlated with degree of NIMO response. Conclusions: These data suggest that baseline anterior paralimbic and prefrontal hypermetabolism may be associated with CBZ response, and hypometabolism with NIMO response. Based on these preliminary data, further exploration of relationships between baseline PET scans and treatment responses is indicated.

AB - Background: Positron emission tomography (PET) studies have reported baseline (medication free) differences between mood disorder patients and healthy control subjects, but relatively little is known about relationships between baseline PET scans and treatment responses. Carbamazepine (CBZ) and to a more limited extent nimodipine (NIMO) seem useful in mood disorders. We explored whether baseline regional cerebral glucose metabolism (rCMRglu) could discriminate CBZ and NIMO responders from nonresponders and healthy control subjects. Methods: In refractory mood disorder patients, we examined relationships between responses to these drugs, assessed by Clinical Global Impression-Improvement scores, and baseline rCMRglu, determined with fluorine-18 deoxyglucose and PET. Results: CBZ responders had baseline left insular hypermetabolism compared to healthy control subjects and nonresponders, whereas nonresponders had widespread (including left insular) hypometabolism. Degree of CBZ response correlated with baseline paralimbic (including insula) and prefrontal hypermetabolism. In responders but not nonresponders, CBZ decreased widespread metabolism, with the degree of decrease in left insula correlating with response. In contrast, NIMO responders but not nonresponders had baseline widespread (including left insular) hypometabolism. Left prefrontal and left insular baseline hypometabolism, but not metabolic changes with treatment correlated with degree of NIMO response. Conclusions: These data suggest that baseline anterior paralimbic and prefrontal hypermetabolism may be associated with CBZ response, and hypometabolism with NIMO response. Based on these preliminary data, further exploration of relationships between baseline PET scans and treatment responses is indicated.

KW - Carbamazepine

KW - Cerebral

KW - Metabolism

KW - Mood disorders

KW - Nimodipine

KW - PET

UR - http://www.scopus.com/inward/record.url?scp=0032703836&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032703836&partnerID=8YFLogxK

U2 - 10.1016/S0006-3223(99)00210-3

DO - 10.1016/S0006-3223(99)00210-3

M3 - Article

C2 - 10578451

AN - SCOPUS:0032703836

VL - 46

SP - 1364

EP - 1374

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 10

ER -