Neurochemical correlates of behavioral treatment of pediatric trichotillomania.
Behavioral treatment
Children
GABA
Glutamate
MRS
Trichotillomania (hair-pulling disorder)
Journal
Journal of affective disorders
ISSN: 1573-2517
Titre abrégé: J Affect Disord
Pays: Netherlands
ID NLM: 7906073
Informations de publication
Date de publication:
01 08 2020
01 08 2020
Historique:
received:
20
11
2019
revised:
30
03
2020
accepted:
27
04
2020
entrez:
21
6
2020
pubmed:
21
6
2020
medline:
16
2
2021
Statut:
ppublish
Résumé
Trichotillomania (TTM) is a chronic and impairing psychiatric disorder with suspected dysfunctional cortico-striato-thalamo-cortical (CSTC) circuit activity reflecting excitatory/inhibitory signaling imbalance. TTM neurochemistry is understudied, with no prior research using magnetic resonance spectroscopy (MRS). This pilot investigation examined associations between TTM diagnosis, symptom severity, and response to behavioral treatment with MRS neurometabolites glutamate (Glu) and γ-aminobutyric acid (GABA) in CSTC structures. Proton echo-planar spectroscopic imaging (PEPSI) MRS was acquired from bilateral pregenual anterior cingulate cortex (pACC), caudate, putamen, globus pallidus, thalamus, and proximal white matter in 10 unmedicated girls with TTM, ages 9-17 years, before and after treatment, and from 13 age- and sex-matched healthy controls. Nine of 10 TTM patients were treatment responders. Pretreatment mean Glu and GABA did not differ significantly between participants and controls. Pretreatment TTM symptoms were correlated with Glu in (left + right) pACC (r = 0.88, p = 0.02) and thalamus (r = 0.82, p = 0.012), and were negatively correlated with pACC GABA (r = -0.84, p = 0.034). Mean GABA in putamen increased 69% (baseline to post-treatment) (p = 0.027). Higher pretreatment Glu in caudate, putamen, globus pallidus, and thalamus predicted greater symptom decreases with treatment (all r < -0.6, p < 0.05); higher caudate GABA predicted less treatment-related symptom decline (r = 0.86, p = 0.014). Small sample, GABA quantified with spectral fitting rather than editing. Consistent with other neuroimaging, MRS reveals discrete CSTC chemical changes with effective behavior therapy, and possibly with TTM etiology. TTM symptoms relate to excess excitatory versus inhibitory signaling in pACC and thalamus; symptom improvement may reflect reduced excitatory drive of the CSTC direct-pathway activity.
Sections du résumé
BACKGROUND
Trichotillomania (TTM) is a chronic and impairing psychiatric disorder with suspected dysfunctional cortico-striato-thalamo-cortical (CSTC) circuit activity reflecting excitatory/inhibitory signaling imbalance. TTM neurochemistry is understudied, with no prior research using magnetic resonance spectroscopy (MRS). This pilot investigation examined associations between TTM diagnosis, symptom severity, and response to behavioral treatment with MRS neurometabolites glutamate (Glu) and γ-aminobutyric acid (GABA) in CSTC structures.
METHODS
Proton echo-planar spectroscopic imaging (PEPSI) MRS was acquired from bilateral pregenual anterior cingulate cortex (pACC), caudate, putamen, globus pallidus, thalamus, and proximal white matter in 10 unmedicated girls with TTM, ages 9-17 years, before and after treatment, and from 13 age- and sex-matched healthy controls.
RESULTS
Nine of 10 TTM patients were treatment responders. Pretreatment mean Glu and GABA did not differ significantly between participants and controls. Pretreatment TTM symptoms were correlated with Glu in (left + right) pACC (r = 0.88, p = 0.02) and thalamus (r = 0.82, p = 0.012), and were negatively correlated with pACC GABA (r = -0.84, p = 0.034). Mean GABA in putamen increased 69% (baseline to post-treatment) (p = 0.027). Higher pretreatment Glu in caudate, putamen, globus pallidus, and thalamus predicted greater symptom decreases with treatment (all r < -0.6, p < 0.05); higher caudate GABA predicted less treatment-related symptom decline (r = 0.86, p = 0.014).
LIMITATIONS
Small sample, GABA quantified with spectral fitting rather than editing.
CONCLUSION
Consistent with other neuroimaging, MRS reveals discrete CSTC chemical changes with effective behavior therapy, and possibly with TTM etiology. TTM symptoms relate to excess excitatory versus inhibitory signaling in pACC and thalamus; symptom improvement may reflect reduced excitatory drive of the CSTC direct-pathway activity.
Identifiants
pubmed: 32560953
pii: S0165-0327(19)33126-X
doi: 10.1016/j.jad.2020.04.061
pii:
doi:
Substances chimiques
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
552-561Subventions
Organisme : NIMH NIH HHS
ID : R01 MH081864
Pays : United States
Informations de copyright
Copyright © 2020. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of Competing Interest Dr. Peris receives funding from the National Institutes of Mental Health (NIMH) and the TLC Foundation for Body Focused Repetitive Behavior and royalties from Oxford University Press. Dr. McCracken reports receiving consultant income from Roche, Octapharma, and GW Biosciences; research clinical trial contracts from Roche, Think Now, Inc, and NICHD; and payment for expert witness participation for Lannett Pharmaceuticals. Dr. Piacentini has received grant or research support from NIMH, the TLC Foundation for Body-focused Repetitive Behaviors, the Tourette Association of America, and Pfizer Pharmaceuticals through the Duke University Clinical Research Institute Network. He receives publication royalties from Guilford Press and Oxford University Press. He receives speaking honoraria and/or travel support from the Tourette Association of America, the International Obsessive Compulsive Disorder Foundation, and the TLC Foundation for Body-focused Repetitive Behaviors.