fMRI and Pathological Gambling Table 1. Changes in Study Measures of the Patient with Pathological Gambling Treated with Fluvoxamine Baseline 1 week* 6 weeks* 6 months* 9 months* BDI 38 36 30 26 25 STAI 54, 52 54, 48 50, 45 42, 43 48, 44 GSAS 48 30 18 8 4 BDI, Beck’s depression inventory; STAI, State-Trait Anxiety Inventory; GSAS, Gambling Symptom Assessment Scales. *After administration of fluvoxamine. Fig. 3. fMRI six weeks after fluvoxamine administration. The figure shows the difference between the activation and resting conditions. There were activated regions in the left frontal (Brodmann’s area 6), right parietal (Brodmann’s areas 7, 40), and left parietal (Brodmann’s areas 7, 19, and 40) lobes. Fig. 4. fMRI six months after fluvoxamine administration. The figure shows the difference between the activation and resting conditions. The previously activated regions were generally decreased. There were small activated regions in the right frontal lobe (Brodmann’s area 6), left occipital lobe (Brodmann’s areas 18, 19), right limbic area (Brodmann’s area 24), and left limbic area (Brodmann’s area 31). effects of the medication. Beck’s Depression Inventory (BDI), State-Trait Anxiety Inventory (STAI), and GSAS had been administered before medication, and they were re- examined on the seventh day after medication. The second fMRI scan was also obtained on the seventh day after medication (Fig. 2). Three weeks after discharge (six weeks after beginning of the fluvoxamine prescription), BDI, STAI, and GSAS were again administered, and the same assessments were also carried out at six and nine months after beginning of the medication (Table 1). Additionally, fMRI scans took place at six weeks and six months after medication (Figs. 3 and 4). The patient did not undergo individual or group cognitive behavioral therapy, nor did he participate in Gamblers Anonymous during or after his admission to the hospital. He had not gone to gamble during the follow-up period. He also had reported that his desire to gamble had decreased, and he was disabused of his unreasonable belief that he could regain his losses by gambling. He presently main- tained his job and social relationships stably after treatment. fMRI was performed on a 1.5T magnetic resonance scanner (Magnetom VISION, Siemens, Erlangen, Germany). For functional imaging, echo-planar imaging (EPI) was used (matrix = 64×64). Five rest conditions were alternated with five activation conditions, and each period consisted of 120 images at 22-second intervals (repetition time). These 1,200 images were collected and analyzed according to the time. During the activation period, the stimuli consisted of card pictures showing a full house, four-of-a-kind, and a royal straight flush. During the resting period, the patient was shown landscape pictures. Analysis of the images from the activation period was performed using SPM 99 statistical parametric mapping software to establish reference vectors corresponding to activation and resting periods. Among regions in which changes in signal intensity were cross- correlated with the reference vector, only regions meeting a threshold of p = .0001 and an extent threshold of 30 voxels (size 2×2×2 mm) were considered as significant signals. The anatomical locations of the activated foci were assigned using the Talairach atlas and were then presented as the appropriate Brodmann’s areas. DISCUSSION Sociological and individual factors have been implicated in the development and maintenance of pathological gambling behavior. Recently, the etiology of pathological gambling has been suggested to involve abnormalities in certain neurotransmitters. Although an understanding of the neu- robiology of pathological gambling is still in its infancy, several recent studies support these theories. Dysfunction of Yonsei Med J http://www.eymj.org Volume 50 Number 3 June 2009 443