Glucose hypermetabolism in the thalamus of patients with drug-induced blepharospasm.
We examined the difference in cerebral function alterations between drug-induced blepharospasm patients and essential blepharospasm (EB) patients by using positron emission tomography with (18)F-fluorodeoxyglucose. Cerebral glucose metabolism was examined in 21 patients with drug-induced blepharospasm (5 men and 16 women; mean age, 53.1 [range, 29-78] years), 21 essential EB patients (5 men and 16 women; mean age, 53.0 [range, 33-72] years) and 24 healthy subjects (6 men and 18 women; mean age, 57.9 [range, 22-78] years) with long-term history of benzodiazepines use (drug healthy subjects). Drug-induced blepharospasm patients developed symptoms while taking benzodiazepines or thienodiazepines. Sixty-three normal volunteers (15 men and 48 women; mean age, 53.6 [range, 20-70] years) were examined as controls. Differences between the patient groups and control group were examined by statistical parametric mapping. Additionally, we defined regions of interests on both sides of the thalamus, caudate nucleus, anterior putamen, posterior putamen and primary somatosensory area. The differences between groups were tested using two-sample t-tests with Bonferroni correction for multiple comparisons. Cerebral glucose hypermetabolism on both side of the thalamus was detected in drug-induced blepharospasm, EB patients and drug healthy subjects by statistical parametric mapping. In the analysis of regions of interest, glucose metabolism in both sides of the thalamus in the drug-induced blepharospasm group was significantly lower than that in the EB group. Moreover, we observed glucose hypermetabolism in the anterior and posterior putamen bilaterally in EB group but not in drug-induced blepharospasm group and drug healthy subjects. Long-term regimens of benzodiazepines or thienodiazepines may cause down-regulation of benzodiazepine receptors in the brain. We suggest that the functional brain alteration in drug-induced blepharospasm patients is similar to that in EB patients, and that alteration of the GABAergic system might be related to the pathology of both blepharospasm types.
Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan; Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan; All Japan Federation of Social Insurance Associations Mishima Hospital, Mishima, Japan. Electronic address: suzuki@f8.dion.ne.jp.
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Suzuki
Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan; Kiyosawa Eye Clinic, Tokyo, Japan.
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Kiyosawa
Inouye Eye Hospital, Tokyo, Japan.
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Wakakura
Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, Graduate School, Tokyo, Japan.
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Mochizuki
Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
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Ishiwata
Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
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Oda
Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
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Ishii
D000328:Adult; D000368:Aged; D001381:Azepines / Q000009:adverse effects*; D001569:Benzodiazepines / Q000009:adverse effects*; D001764:Blepharospasm / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000378:metabolism*; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D013788:Thalamus / Q000000981:diagnostic imaging / Q000378:metabolism*; D055815:Young Adult
D001381:Azepines; D001569:Benzodiazepines; D005947:Glucose
GABAergic system; benzodiazepines; blepharospasm; brain metabolism; dystonia