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Background: Effective management of Hoarding Disorder (HD) must begin with assessment of the severity of hoarding symptoms and functional impairment. We sought to validate the UCLA Hoarding Severity Scale (UHSS), a semi-structured, clinician-administered rating scale that measures the severity of both the core symptoms of HD and the associated features of indecisiveness, perfectionism, task prolongation, and procrastination, which are significantly associated with the diagnosis and impairment of HD., Methods: Hoarding symptom severity was measured in 62 patients who met DSM-5 diagnostic criteria for HD and 65 normal controls, using the UHSS and the Saving Inventory-Revised (SI-R), a well validated self-report measure of hoarding symptoms., Results: The UHSS showed significant internal consistency (Cronbach׳s α=.70). Principal components analysis revealed three factors that accounted for 58% of the variance: 1) associated features and functional impairment, 2) clutter volume and social impairment, and 3) difficulty discarding, urges to save, and excessive acquisition. UHSS and SI-R scores were significantly correlated. UHSS and SI-R total and factor scores of HD patients were all significantly different from those of controls., Limitations: Inter-rater and test-retest reliability were not assessed. The initial version of the UHSS did not contain rater instructions, so it lacked quantifiable anchor points for ratings., Conclusions: The UHSS showed internal consistency, construct validity, convergent validity, and known groups discriminant validity. The UHSS validly measures the core symptoms, associated features, and functional impairment of patients with HD. Utilizing a valid clinician-administered scale will provide a more comprehensive and accurate clinical assessment of patients with HD., (Copyright © 2015 Elsevier B.V. All rights reserved.)

The neurophysiological bases of cognitive-behavioral therapy (CBT) for obsessive-compulsive disorder (OCD) are incompletely understood. Previous studies, though sparse, implicate metabolic changes in pregenual anterior cingulate cortex (pACC) and anterior middle cingulate cortex (aMCC) as neural correlates of response to CBT. The goal of this pilot study was to determine the relationship between levels of the neurochemically interlinked metabolites glutamate + glutamine (Glx) and N-acetyl-aspartate + N-acetyl-aspartyl-glutamate (tNAA) in pACC and aMCC to pretreatment OCD diagnostic status and OCD response to CBT. Proton magnetic resonance spectroscopic imaging ((1)H MRSI) was acquired from pACC and aMCC in 10 OCD patients at baseline, 8 of whom had a repeat scan after 4 weeks of intensive CBT. pACC was also scanned (baseline only) in 8 age-matched healthy controls. OCD symptoms improved markedly in 8/8 patients after CBT. In right pACC, tNAA was significantly lower in OCD patients than controls at baseline and then increased significantly after CBT. Baseline tNAA also correlated with post-CBT change in OCD symptom severity. In left aMCC, Glx decreased significantly after intensive CBT. These findings add to evidence implicating the pACC and aMCC as loci of the metabolic effects of CBT in OCD, particularly effects on glutamatergic and N-acetyl compounds. Moreover, these metabolic responses occurred after just 4 weeks of intensive CBT, compared to 3 months for standard weekly CBT. Baseline levels of tNAA in the pACC may be associated with response to CBT for OCD. Lateralization of metabolite effects of CBT, previously observed in subcortical nuclei and white matter, may also occur in cingulate cortex. Tentative mechanisms for these effects are discussed. Comorbid depressive symptoms in OCD patients may have contributed to metabolite effects, although baseline and post-CBT change in depression ratings varied with choline-compounds and myo-inositol rather than Glx or tNAA., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Compulsive hoarding patients have been found in previous studies to have substantial disability and functional impairment. However, no prior study has examined subjective and objective quality of life (QOL) in patients with compulsive hoarding. This present study compared compulsive hoarders and non-hoarding OCD patients across a variety of QOL domains. Subjects were 171 consecutive adult patients (34 compulsive hoarders, 137 non-hoarding patients with DSM-IV OCD) treated openly between 1998 and 2004 in the UCLA OCD Partial Hospitalization Program (OCD PHP), a specialized, intensive, multi-modal treatment program for treatment-refractory patients. Scores on the Quality of Life Scale and other symptom severity measures on admission were compared between compulsive hoarders and non-hoarding OCD patients. Compulsive hoarders were older and had lower global functioning than non-hoarding OCD patients. Both groups had low overall QOL scores across multiple domains. Compulsive hoarders had significantly lower levels of satisfaction with their safety than non-hoarding OCD patients, were more often the victims of both violent and non-violent crime, felt less safe in their neighborhoods, and felt less protected against attack. Compulsive hoarders were also much less satisfied with their living arrangements than non-hoarding OCD patients. No differences were found on financial variables, but the vast majority of patients in both groups were unemployed. Compulsive hoarders have lower QOL than non-hoarding OCD patients in the domains of safety and living situation. Psychosocial rehabilitation that focuses on problems with victimization, safety, employment, and financial areas may be a beneficial augmentation to treatment for compulsive hoarding., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Objective: Compulsive hoarding, found in many patients with obsessive-compulsive disorder (OCD), has been associated with poor response to serotonin reuptake inhibitor (SRI) medications in some reports. However, no prior study has quantitatively measured response to standardized pharmacotherapy in compulsive hoarders. We sought to determine whether compulsive hoarders would respond as well as non-hoarding OCD patients to the SRI, paroxetine., Methods: Seventy-nine patients with OCD (32 patients with the compulsive hoarding syndrome and 47 patients without prominent hoarding symptoms) were treated openly with paroxetine (mean dose 41.6+/-12.8 mg/day; mean duration 80.4+/-23.5 days) according to a standardized protocol, from 3/1993 to 7/2005. All subjects were free of psychotropic medication for at least four weeks prior to study entry. No psychotherapy or psychotropic medications except paroxetine were allowed during the study period. Subjects were assessed before and after treatment with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Hamilton Depression Rating Scale (HDRS), Hamilton Anxiety Scale (Ham-A), Global Assessment Scale (GAS), and Clinical Global Impression/Improvement (CGI) scale., Results: Both compulsive hoarders and non-hoarding OCD patients improved significantly with treatment (p<0.001), with nearly identical changes in Y-BOCS, HDRS, Ham-A, and GAS scores. There were no significant differences between groups in the proportions of patients who completed or responded to treatment. Hoarding symptoms improved as much as other OCD symptoms., Conclusions: Compulsive hoarders responded as well to paroxetine treatment as non-hoarding OCD patients, suggesting that SRI medications are effective for compulsive hoarding. Controlled trials of SRI medications for compulsive hoarding are now warranted.

Compulsive hoarding and saving symptoms, found in many patients who have obsessive-compulsive disorder (OCD), are part of a clinical syndrome that has been associated with poor response to antiobsessional medications and cognitive-behavioral therapy (CBT). Specific CBT strategies targeting the characteristic features of the compulsive hoarding syndrome have had better results. This article provides an overview of the compulsive hoarding syndrome, a review of treatment approaches and their efficacy, a case presentation, and a detailed discussion of intensive, multimodal CBT for compulsive hoarding. New insights into the neurobiological characteristics of compulsive hoarding that might direct future treatment development are also presented.

Objective: Compulsive hoarding and saving symptoms, found in many patients with obsessive-compulsive disorder (OCD), are part of a discrete clinical syndrome that includes indecisiveness, disorganization, perfectionism, procrastination, and avoidance and has been associated with poor response to medications and cognitive behavior therapy. The authors sought to identify cerebral metabolic patterns specifically associated with the compulsive hoarding syndrome using positron emission tomography (PET)., Method: [(18)F]Fluorodeoxyglucose PET scans were obtained for 45 adult subjects who met DSM-IV criteria for OCD (12 of whom had compulsive hoarding as their most prominent OCD symptom factor) and 17 normal comparison subjects. All subjects had been free of psychotropic medication for at least 4 weeks. Regional cerebral glucose metabolism was compared between the groups., Results: In relation to the comparison subjects, the patients with compulsive hoarding syndrome had significantly lower glucose metabolism in the posterior cingulate gyrus and cuneus, whereas the nonhoarding OCD patients had significantly higher glucose metabolism in the bilateral thalamus and caudate. In relation to nonhoarding OCD patients, compulsive hoarders had significantly lower metabolism in the dorsal anterior cingulate gyrus. Across all OCD patients, hoarding severity was negatively correlated with glucose metabolism in the dorsal anterior cingulate gyrus., Conclusions: OCD patients with the compulsive hoarding syndrome had a different pattern of cerebral glucose metabolism than nonhoarding OCD patients and comparison subjects. Obsessive-compulsive hoarding may be a neurobiologically distinct subgroup or variant of OCD whose symptoms and poor response to anti-obsessional treatment are mediated by lower activity in the cingulate cortex.

Background: The purpose of this study was to explore the efficacy of adding an atypical antipsychotic, olanzapine, to a serotonin reuptake inhibitor (SRI) in treatment-refractory obsessive-compulsive disorder (OCD)., Method: Twenty-six patients aged between 18 and 65 (mean = 41.2, SD = 11.9) years meeting DSM-IV criteria for OCD, who had not responded to SRIs, were treated for 6 weeks in a double-blind, placebo-controlled augmentation study with either olanzapine (up to 20 mg/day) or placebo. Severity of illness was assessed biweekly by the Yale-Brown Obsessive Compulsive Scale (Y-BOCS). Analysis of covariance with baseline Y-BOCS score included as a covariate was used to compare improvement in Y-BOCS scores in the 2 groups. Response was defined as a 25% or greater improvement in Y-BOCS score. Data were collected between April 2001 and May 2003., Results: Outcome was assessed for all patients using the last observation carried forward. Subjects in the olanzapine group had a mean decrease of 4.2 (SD = 7.9) in Y-BOCS score compared with a mean increase in score of 0.54 (SD = 1.31) for subjects in the placebo group (F = 4.85, df = 2,23; p =.04). Six (46%) of 13 subjects in the olanzapine group showed a 25% or greater improvement in Y-BOCS score compared with none in the placebo group. The final mean dose of olanzapine was 11.2 (SD = 6.5) mg/day. Medication was well tolerated. Only 2 (15%) of 13 subjects who received olanzapine discontinued because of side effects: sedation (N = 1) or weight gain (N = 1)., Conclusion: These results provide preliminary evidence that adding olanzapine to SRIs is potentially efficacious and well tolerated in the short-term treatment of patients with refractory OCD. Controlled studies with larger sample sizes are necessary to more definitively address this treatment strategy.

Objective: Serotonin reuptake inhibitor (SRI) medications are effective in the treatment of both major depressive disorder and obsessive-compulsive disorder (OCD), but it is unknown whether the neural substrates of treatment response for the two disorders are the same or different. The authors sought to identify pretreatment cerebral glucose metabolic markers of responsiveness to SRI treatment in patients with OCD versus major depressive disorder and to determine whether the pretreatment patterns associated with improvement of OCD symptoms were the same as or different from those associated with improvement of major depressive disorder symptoms., Method: [(18)F]Fluorodeoxyglucose positron emission tomography was used to measure cerebral glucose metabolism in 27 patients with OCD alone, 27 with major depressive disorder alone, and 17 with concurrent OCD and major depressive disorder, who were all then treated with 30-60 mg/day of paroxetine for 8-12 weeks. Correlations were calculated between pretreatment regional metabolism and pre- to posttreatment changes in the severity of OCD symptoms, depressive symptoms, and overall functioning., Results: While improvement of OCD symptoms was significantly correlated with higher pretreatment glucose metabolism in the right caudate nucleus (partial r=-0.53), improvement of major depressive disorder symptoms was significantly correlated with lower pretreatment metabolism in the amygdala (partial r=0.71) and thalamus (partial r=0.34) and with higher pretreatment metabolism in the medial prefrontal cortex and rostral anterior cingulate gyrus (Talairach coordinates: x=0, y=62, z=10) (z=2.91)., Conclusions: These findings suggest that, although both OCD and major depressive disorder respond to SRIs, the two syndromes have different neurobiological substrates for response. Elevated activity in the right caudate may be a marker of responsiveness to antiobsessional treatment, while lower right amygdala activity and higher midline prefrontal activity may be required for response of depressive symptoms to treatment.

Background: Serotonin reuptake inhibitors (SRIs) effectively treat both major depressive disorder (MDD) and obsessive-compulsive disorder (OCD). We compared and contrasted the functional neuroanatomical effects of SRIs in OCD and MDD as these 2 disorders occurred separately and concurrently by measuring pretreatment to posttreatment cerebral glucose metabolic changes in OCD vs MDD vs concurrent OCD + MDD., Methods: We obtained [(18)F]fluorodeoxyglucose positron emission tomography (PET) brain scans on 25 subjects with OCD, 25 with MDD, and 16 with concurrent OCD + MDD before and after 8 to 12 weeks of treatment with paroxetine hydrochloride. Controls (n = 16) were scanned 10 to 12 weeks apart without treatment. Treatment response was defined as a more than 25% decline in OCD symptom severity, a more than 50% decline in MDD severity, and "much improved" clinical global impression., Results: Although all patient groups received the same paroxetine dose for the same duration, regional metabolic changes differed significantly among diagnostic groups. Subjects with OCD alone showed significant metabolic decreases in the right caudate nucleus, right ventrolateral prefrontal cortex (VLPFC), bilateral orbitofrontal cortex, and thalamus that were not seen in any other group. Both the MDD and concurrent OCD + MDD groups showed metabolic decreases in the left VLPFC and increases in the right striatum. Treatment response was associated with a decrease in striatal metabolism in nondepressed OCD patients but with an increase in striatal activity in patients with OCD + MDD., Conclusions: Brain metabolic responses to SRIs are both disorder-specific and response-specific. They vary according to the underlying pathophysiology of the patient and the degree of symptomatic improvement.

Background: Compulsive hoarding and saving symptoms, found in many patients with obsessive-compulsive disorder (OCD), are part of a clinical syndrome that has been associated with poor response to medications and cognitive-behavioral therapy (CBT). We sought to determine whether patients with the compulsive hoarding syndrome had more severe symptoms and functional impairment than nonhoarding OCD patients and whether they would respond to intensive, multimodal treatment previously found to be effective for treatment-refractory OCD., Method: We studied 190 consecutive patients with DSM-IV OCD treated openly for approximately 6 weeks with intensive CBT, medication, and psychosocial rehabilitation in a partial hospitalization program for severely ill OCD patients. Twenty of the 190 patients (11%) were identified as having the compulsive hoarding syndrome. All patients were assessed before and after treatment with the Yale-Brown Obsessive Compulsive Scale (YBOCS), Hamilton Rating Scale for Depression (HAM-D). Hamilton Rating Scale for Anxiety (HAM-A). and Global Assessment Scale (GAS). We compared the symptom severity and response to treatment of compulsive hoarders versus nonhoarding OCD patients., Results: Compulsive hoarders were significantly older than nonhoarders (p < .001). Hoarders had significantly lower GAS scores and higher HAM-A scores than nonhoarders both before (p = .04) and after (p = .002) treatment, but had similar pretreatment YBOCS scores. Both groups improved significantly with treatment as assessed by YBOCS score (p < .001), but nonhoarders had significantly greater decreases in YBOCS scores than hoarders (p = .02)., Conclusion: While the compulsive hoarding syndrome appears to be a distinct, more disabling, variant of OCD that does not respond as robustly to treatment, it may still improve significantly with intensive, multimodal treatment tailored to its specific features and associated deficits.

Background: The frequent comorbidity of major depressive disorder (MDD) and obsessive-compulsive disorder (OCD) suggests a fundamental relationship between them. We sought to determine whether MDD and OCD have unique cerebral metabolic patterns that remain the same when they coexist as when they occur independently., Methods: [18F]-fluorodeoxyglucose positron emission tomography (PET) brain scans were obtained on 27 subjects with OCD alone, 27 with MDD alone, 17 with concurrent OCD+MDD, and 17 normal control subjects, all in the untreated state. Regional cerebral glucose metabolism was compared between groups., Results: Left hippocampal metabolism was significantly lower in subjects with MDD alone and in subjects with concurrent OCD+MDD than in control subjects or subjects with OCD alone. Hippocampal metabolism was negatively correlated with depression severity across all subjects. Thalamic metabolism was significantly elevated in OCD alone and in MDD alone. Subjects with concurrent OCD+MDD had significantly lower metabolism in thalamus, caudate, and hippocampus than subjects with OCD alone., Conclusions: Left hippocampal dysfunction was associated with major depressive episodes, regardless of primary diagnosis. Other cerebral metabolic abnormalities found in OCD and MDD occurring separately were not seen when the disorders coexisted. Depressive episodes occurring in OCD patients may be mediated by different basal ganglia-thalamic abnormalities than in primary MDD patients.

Background: Human and animal studies point to 3 dimensions of personality that change during pharmacotherapy with a selective serotonin reuptake inhibitor (SSRI). Specifically, harm avoidance has been found to decrease, social dominance has been found to increase, and hostility in social situations has been found to decrease with SSRI treatment. We sought to determine personality changes in subjects with either major depressive disorder (MDD) or obsessive-compulsive disorder (OCD) treated with paroxetine. We also sought to determine whether or not these personality changes were associated with disease state (MDD vs. OCD) or treatment response (responders vs. nonresponders)., Method: Thirty-seven subjects diagnosed with either MDD or OCD (according to DSM-IV criteria) completed the Cattell 16 Personality Factor Inventory (16-PF) before and after treatment with paroxetine. Treatment response was defined as a Clinical Global Impressions-Improvement rating of "much" or "very much" improved and a drop in Hamilton Rating Scale for Depression score of at least 50% for MDD or Yale-Brown Obsessive Compulsive Scale score of at least 30% for OCD., Results: No significant differences were found between subjects with MDD and OCD in personality change with treatment. In the whole group, treatment responders had a greater decrease than nonresponders in 16-PF factors relating to harm avoidance. An increase in social dominance factors and a decrease in factors relating to hostility in social situations were found, but these changes were not significantly different between responders and nonresponders., Conclusion: These findings indicate that certain personality dimensions change with SSRI treatment and that some of these changes are independent of clinical treatment response.

Previous positron emission tomography (PET) studies of patients with obsessive-compulsive disorder (OCD) have found elevated glucose metabolic rates in the orbitofrontal cortex (OFC) and caudate nuclei that normalize with response to treatment. Furthermore, OCD symptom provocation differentially activates specific subregions of the OFC, which have distinct patterns of connectivity and serve different functions. Therefore, we sought to determine the role of specific subregions of the OFC and associated subcortical structures in mediating OCD symptoms, by determining how glucose metabolism in these structures changed with paroxetine treatment of OCD patients. We also sought to determine whether pretreatment OFC metabolism would predict response to paroxetine, as it has for other OCD treatments. Twenty subjects with OCD received [18F]-fluorodeoxyglucose (FDG)-PET scans before and after 8 to 12 weeks of treatment with paroxetine, 40 mg/day. In patients who responded to paroxetine, glucose metabolism decreased significantly in right anterolateral OFC and right caudate nucleus. Lower pretreatment metabolism in both left and right OFC predicted greater improvement in OCD severity with treatment. These results add to evidence indicating that orbitofrontal-subcortical circuit function mediates the symptomatic expression of OCD. Specific subregions of the OFC may be differentially involved in the pathophysiology of OCD and/or its response to pharmacotherapy.