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Multimodal neurometabolic investigation of the effects of zolpidem on leukoencephalopathy‐related apathy
Author(s) -
Delorme C.,
Adanyeguh I.,
Bendetowicz D.,
Le Ber I.,
Ponchel A.,
Kas A.,
Habert M.O.,
Mochel F.
Publication year - 2020
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.14465
Subject(s) - apathy , zolpidem , orbitofrontal cortex , medicine , basal ganglia , frontal lobe , neuroscience , psychiatry , psychology , cognition , central nervous system , prefrontal cortex , insomnia
Abstract Background and purpose The symptomatic effect of zolpidem on apathy has been reported in neurological disorders such as strokes and post‐anoxic brain injuries, but not in white‐matter disease of the brain. Methods A 38‐year‐old patient presenting with severe apathy related to a genetic leukoencephalopathy but showing marked improvement of apathy after taking 10 mg of zolpidem was studied. To understand what may mediate such a clinical effect, a multimodal neurometabolic approach using 18 F fluorodeoxyglucose positron emission tomography (FDG‐PET) and a dedicated magnetic resonance spectroscopy (MRS) sequence for gamma aminobutyric acid (GABA) and glutamine + glutamate metabolism was undertaken. Results Pre‐zolpidem FDG‐PET showed hypometabolism in the orbitofrontal cortex, dorsolateral cortex and basal ganglia compared to healthy controls. Post‐zolpidem, FDG‐PET displayed increased metabolism in the orbitofrontal cortex together with improvement in the emotional and auto‐activation domains of apathy. There was no improvement in the cognitive domain of apathy, and no change in metabolism in the dorsolateral frontal cortex. Post‐zolpidem, MRS showed increased GABA and glutamine + glutamate levels in the frontal cortex and pallidum. Conclusion Our multimodal neurometabolic study suggests that the effects of zolpidem on apathy are related to increased metabolism in the orbitofrontal cortex and basal ganglia secondary to GABA modulation. Zolpidem may improve apathy in other white‐matter disorders.

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