Use of 18F-FDG positron emission tomography in the diagnosis and evaluation of the efficiency of treatment for resistant anxiety-obsessive disorders

• Published in: Vestnik rentgenologii i radiologii no. 1; p. 24
• Main Authors: Pozdniakov, A V, Tiutin, L A, Stanzhevskiĭ, A A, Korzenev, A V, Kostenikov, N A, Shamreĭ, V K, Abritalin, E Iu
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01.01.2008
• Subjects: Adult; Brain - metabolism; Drug Resistance; Female; Fluorodeoxyglucose F18; Glucose - metabolism; Humans; Male; Obsessive-Compulsive Disorder - diagnostic imaging; Obsessive-Compulsive Disorder - metabolism; Obsessive-Compulsive Disorder - surgery; Positron-Emission Tomography - methods; Radiopharmaceuticals; Radiosurgery - methods; Tourette Syndrome - diagnostic imaging; Tourette Syndrome - metabolism; Tourette Syndrome - surgery; Treatment Outcome
• ISSN: 0042-4676

The purpose of the investigation was to study the capacities of 18F-FDG positron emission tomography (PET) in the diagnosis and evaluation of the efficiency of treatment for resistant anxiety-obsessive disorders (AOD). 18F-FDG PET was performed in 21 patients with AOD. In 17 cases, the studies were made before and after therapy. Fourteen patients underwent stereotactic surgical intervention. Pretreatment 18F-FDG PET showed that the patients with AOD had hypermetabolism in the cingulated gyri, caudate nuclei, and thalamus in 7, 8, and 6 cases, respectively. A varying clinical improvement (by the Y-OCS and Spilberger scales) was observed in all the examinees after complex or drug treatment throughout the follow-up. According to the data of PET, these patients were observed to have significantly reduced metabolism of glucose in the anterior cingulated guri and its increased metabolism in the heads of the caudate nuclei and thalamus. The metabolic changes detected by PET are strongly and moderately correlated with the pattern of a clinical picture (p < 0.05). It is concluded that the use of 18F-FDG PET makes it possible to provide more accurate insight into the pathogenetic mechanisms responsible for the development of AOD, to objectify the choice of targeted intracerebral structures in order to perform stereotactic neurosurgical interventions, and to optimize drug therapy and to evaluate the efficiency of the treatment performed in early periods.