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Treatment of late-onset OCD following basal ganglia infarct
Abstract
Current consensus on the treatment of obsessive-compulsive disorder (OCD) includes cognitive behavior therapy (CBT) in the form of exposure and response prevention (ERP). However, the generalizability of these methods to elderly populations remains largely undocumented. This clinical case study examines the effectiveness of medications and intensive, inpatient ERP in an elderly patient with onset of OCD following basal ganglia infarcts. There was a dramatic reduction from baseline to follow-up in both obsessions and compulsions with Yale-Brown Obsessive-Compulsive Scale [YBOCS; Goodman et al., 1989] total scores decreasing by over 20 points. These gains were maintained up to 1 year post-treatment. Age-specific issues and the application of standard therapeutic methods to elderly clients are discussed.
... Clinical work early on suggested that dysfunction of the striatum might be important in the emergence of OCD symptoms. Comorbid OCD symptoms were identified in neurodegenerative disorders such as Parkinson's disease and Huntington's disease181920, and in the wake of focal lesions in the caudate nucleus produced by infarcts [21]. New clinical evidence supports this connection between striatum-related circuits and OCD symptoms. ...
... For example, the most widely applied treatments for OCD patients are pharmacologic therapy with selective serotonin-reuptake inhibitors (SSRI) and cognitive behavioral therapy (CBT). Neuroimaging studies reported differentially decreased activity in the striatum and associated cortical regions including the OFC after these treatments [21,22]. Further evidence implicating striatal circuitry in OCD is being obtained with the therapeutic use of deep brain stimulation (DBS) targeting subcortical structures to treat severely ill OCD patients for whom conventional treatments have proved ineffective. ...
Increasing evidence implicates abnormalities in corticostriatal circuits in the pathophysiology of obsessive-compulsive disorder (OCD) and OC-spectrum disorders. Parallels between the emergence of repetitive, compulsive behaviors and the acquisition of automated behaviors suggest that the expression of compulsions could in part involve loss of control of such habitual behaviors. The view that striatal circuit dysfunction is involved in OC-spectrum disorders is strengthened by imaging and other evidence in humans, by discovery of genes related to OCD syndromes, and by functional studies in animal models of these disorders. We highlight this growing concordance of work in genetics and neurobiology suggesting that frontostriatal circuits, and their links with basal ganglia, thalamus and brainstem, are promising candidates for therapeutic intervention in OCD.
... However, individuals over the age of 65 years have generally been excluded from these treatment trials [19][20][21]. As such, the generalisability of these methods to elderly populations remains largely undocumented [22]. Instead, the management of anxiety in this population is likely to be extrapolated from research employing younger age group, or based on personal clinical experience [23]. ...
... Several researchers have also demonstrated in single case studies the efficacy of ERP when combined with other OCD treatment approaches. These have included ERP with pharmacotherapy for older adults who developed late onset OCD following a basal ganglia infarct [22], or following stressful life events [25]. Hirsch et al. [26] demonstrated the effectiveness of a combined approach that included both ERP and cognitive interventions for an 80-year old man who had experienced OCD for 50 years. ...
Obsessive compulsive disorder (OCD) is one of the most frequently occurring psychiatric conditions in older adults. While exposure and response prevention (ERP) is considered the most effective psychological treatment for children and adults with OCD, research investigating its effectiveness for older adults is scarce. This clinical case study investigates the effectiveness of ERP in an 80-year-old man with a 65-year history of OCD. The client received 14 individual, 50-minute ERP treatment sessions. Clinician-based Y-BOCS scores reduced by 65% from 20 (moderate) at pretreatment to 7 (subclinical) at 7-month posttreatment followup. OCI-R total scores reduced by 45% from 38 at baseline to 21 at 7-month follow-up. Despite his long history of the disorder, ERP was effective and well tolerated. The application of ERP for older adults with OCD, including age-specific modifications that may be required for this treatment approach, is discussed.
... Studies investigating the pathophysiology of OCD are very important because they ultimately shed light on treatment strategies. There are case reports presenting OCD following orbito-frontal cortex, [1] basal ganglia, [2] and thalamic lesions. [3] Neurobiology of OCD includes abnormalities of the corticostriatal-thalamocortical loop. ...
Obsessive compulsive disorder (OCD) is a common neuropsychiatric disorder involving predominantly the cortico-striato-thalamo-cortical loop. Although it is usually associated with various disorders of basal ganglia and thalamus, it is difficult to say what kind of impairment causes this situation exactly. Structural brain lesions may be one of the rare causes of refractory psychiatric symptoms. Analysis of such type of cases gives an idea about the neurobiology of psychiatric diseases. In this manuscript, we presented a case of refractory OCD with symptoms regressing after thalamic infarction and discussed with relevant literature.
... Previous studies have shown that MDA reduces levels of serotonin in the brain [49]. OCD symptoms also result from some damages in the dopamine receptor-rich basal ganglia [50]. Also, OXS could at first be adaptive through enhancement of NT. ...
Background
This meta-analysis aimed to investigate serum and plasma malondialdehyde (MDA) levels in patients with obsessive–compulsive disorder (OCD) in comparison to healthy controls.
Methods
Following the PRISMA protocol, we searched for the relevant studies through the databases of Scopus, PubMed, Google Scholar, and web of science until September 2019 with no time restriction. Overall, nine studies were included in the current meta-analysis. Data were pooled using a random-effects model; in addition, standard mean difference (SMD) and/or weight mean difference (WMD) was calculated. Cochran’s Q test and I-square (I ² ) statistics were used to evaluate between-study heterogeneity. The Newcastle–Ottawa scale (NOS) was used to evaluate the quality of the included studies. Statistical analyses were done using the STATA version 14.
Results
Our systematic review included nine case–control studies (including 367 cases and 337 controls). Pooling findings from these studies showed a significantly higher MDA level in OCD patient compared to control groups (SMD = 1.62; 95% CI [0.53, 2.72]; I ² = 96.9%; Pheterogeneity (Ph) < 0.001). This finding remained unchanged among studies which reported MDA in the same unit (WMD = 1.93; 95% CI [0.27, 3.59]; I ² = 99.2%; Ph < 0.001). Subgroup analysis by the study location and sample size revealed findings that were also significant.
Conclusion
We found that MDA levels are higher in OCD patients than healthy controls. This finding highlights the importance of inflammatory responses in OCD patients that should be considered for future investigations. Further studies are recommended to expand current knowledge on this issue.
... There is extensive interaction between the dopamine and serotonin systems, particularly in the basal ganglia (Parent, Wallman, Gagnon, & Parent, 2011), an area consistently implicated in OCD by neuroimaging studies (Del Casale et al., 2011;Sakai et al., 2011;Welter et al., 2011). Functional changes to basal ganglia activity correlate with clinical improvement in OCD patients (Nakao, Okada, & Kanbda, 2014), and insults to this area are known to produce OCD symptoms (Asbahr et al., 2005;Carmin, Wiegartz, Yunus, & Gillock, 2002;Thobois, Jouanneau, Bouvard, & Sindou, 2004). ...
The recent revivification of interest in the therapeutic use of psychedelics has had a particular focus on mood disorders and addiction, although there is reason to think these drugs may be effective more widely. After outlining pertinent aspects of psilocybin and obsessive-compulsive disorder (OCD), the current review summarizes the evidence indicating that there may be a role for psilocybin in the treatment of OCD, as well as highlighting a range of potential therapeutic mechanisms that reflect the action of psilocybin on brain function. Although the current evidence is limited, that multiple signals point in directions consistent with treatment potential, alongside the psychological and physiological safety of clinically administered psilocybin, support the expansion of research, both in animal models and in further randomized controlled trials, to properly investigate this potential.
... Les neurones de l'aire tegmentale ventrale projettent vers les régions corticales préfrontales via la voie méso-corticale et vers le striatum L'interaction existante entre ces deux systèmes de neurotransmission est une des raisons de l'intérêt porté au système dopaminergique ; l'efficacité des ISRS pouvant reposer en partie sur celui-ci. D'autres arguments viennent à l'appui de son implication dans le TOC comme l'identification dès les années 60 de son rôle dans la genèse de comportements stéréotypés dans le cas de son dysfonctionnement (Randrup & Munkvad, 1967) ; ou bien encore la mise en évidence dès les années 80 de l'implication des régions striatales (à forte innervation dopaminergique) dans la physiopathologie du TOC, leur lésion entrainant l'émergence d'une symptomatologie obsessionnelle et compulsive (Carmin et al., 2002). L'efficacité chez environ 30 % des patients présentant un TOC résistant aux ISRS de stratégies de potentialisation reposant sur l'emploi d'anti-dopaminergiques que sont les antipsychotiques atypiques (Hirschtritt et al., 2017) est aussi un argument en faveur de son implication 28 (Koo et al., 2010). ...
Le trouble obsessionnel-compulsif (TOC) se caractérise par des obsessions (idées intrusives) et des compulsions (comportements répétitifs exécutés au travers de rituels rigides). Cette observation phénoménologique a conduit à explorer l'idée que les patients souffrant de TOC présentent un déficit de flexibilité cognitive ; c’est-à-dire de leur capacité à s'adapter aux changements environnementaux. Ainsi, l'objectif était double : tester l'hypothèse d'un déficit de flexibilité cognitive sous-tendant les comportements compulsifs et explorer leurs bases neurobiologiques chez les patients et un modèle animal de compulsion, les souris Sapap3 KO. Nous avons ainsi développé une tâche de renversement de l'apprentissage similaire dans les deux espèces, et observé que seul un sous-groupe de sujets compulsifs, ce dans les deux espèces, présentaient des performances altérées. Ce déficit trans-espèces n'était pas corrélé à la sévérité des comportements compulsifs et se traduisait non par une plus grande tendance à la persévération après renversement des contingences, mais par une plus grande labilité dans leurs réponses après renversement. La suite de ce travail a consisté à explorer les bases neurales de la flexibilité cognitive et son lien avec la compulsion en modulant les circuits cortico-subthalamiques à la fois chez les patients (par stimulation cérébrale profonde) et les souris Sapap3 KO (par modulation pharmacologique et stimulation optogénétique) pendant la réalisation de la tâche. Bien qu'encore préliminaires, les premières observations tendent vers un déficit de flexibilité cognitive tel que mesuré dans notre tâche comme trait indépendant de la symptomatologie compulsive.
... L'interaction existante entre ces deux systèmes de neurotransmission est une des raisons de l'intérêt porté au système dopaminergique ; l'efficacité des ISRS pouvant reposer en partie sur celui-ci. D'autres arguments viennent à l'appui de son implication dans le TOC comme l'identification dès les années 60 de son rôle dans la genèse de comportements stéréotypés dans le cas de son dysfonctionnement (Randrup & Munkvad, 1967) ; ou bien encore la mise en évidence dès les années 80 de l'implication des régions striatales (à forte innervation dopaminergique) dans la physiopathologie du TOC, leur lésion entrainant l'émergence d'une symptomatologie obsessionnelle et compulsive (Carmin et al., 2002). L'efficacité chez environ 30 % des patients présentant un TOC résistant aux ISRS de stratégies de potentialisation reposant sur l'emploi d'anti-dopaminergiques que sont les antipsychotiques atypiques (Hirschtritt et al., 2017) est aussi un argument en faveur de son implication 27 (Koo et al., 2010). ...
Obsessive-compulsive disorder (OCD) is characterized by obsessions (intrusive ideas) and compulsions (repetitive behaviours performed through rigid rituals). This phenomenological observation led to the exploration of the idea that OCD patients have a deficit of cognitive flexibility, i.e. their ability to adapt to environmental changes. However, the question of whether OCD is associated with a cognitive flexibility impairment remains unresolved with inconsistencies across studies. The use of scales developed to measure this cognitive dimension could positively contribute to the debate by allowing a simple and rapid measurement that can be easily administered to large numbers of patients, unlike experimental measurements. Thus, the objective was twofold: to adapt a french version of two scales measuring this dimension, the Cognitive Flexibility Scale (CFS) and the Cognitive Flexibility Inventory (CFI); to assess the psychometric properties of these scales in non-clinical populations (n = 488) and compare them to an experimental measure of cognitive flexibility, the reversal learning, in both a non-clinical (n = 110) and a clinical population (n = 40 OCD patients). The CFI and CFS have thus demonstrated good psychometric properties. However, although patients scored lower than healthy subjects on these scales, the latter failed to demonstrate good convergent validity with reversal learning, indicating a divergence in the measured constructs. In conclusion, these scales cannot replace experimental measures of cognitive flexibility.
... Interestingly, OFC-striatal circuits are also implicated in compulsive behavioral automaticity. Abnormalities of the structure, connectivity and activity of the caudate (the human DMS) have been observed in OCD patients (Carmin et al., 2002;Guehl et al., 2008;Sakai et al., 2011;Fan et al., 2012). Furthermore, three genetic mouse models of OCD have been characterized (D1CT-7; SAPAP3 −/− and Slitrk5 −/− ), and in each of them, the major circuit phenotype observed has been disruption of cortico-striatal synaptic transmission, particularly involving inputs from OFC (Nordstrom and Burton, 2002;Welch et al., 2007;Shmelkov et al., 2010;Burguière et al., 2013Burguière et al., , 2015. ...
Here, we review the neural circuit bases of habits, compulsions, and addictions, behaviors which are all characterized by relatively automatic action performance. We discuss relevant studies, primarily from the rodent literature, and describe how major headway has been made in identifying the brain regions and neural cell types whose activity is modulated during the acquisition and performance of these automated behaviors. The dorsal striatum and cortical inputs to this structure have emerged as key players in the wider basal ganglia circuitry encoding behavioral automaticity, and changes in the activity of different neuronal cell-types in these brain regions have been shown to co-occur with the formation of automatic behaviors. We highlight how disordered functioning of these neural circuits can result in neuropsychiatric disorders, such as obsessive-compulsive disorder (OCD) and drug addiction. Finally, we discuss how the next phase of research in the field may benefit from integration of approaches for access to cells based on their genetic makeup, activity, connectivity and precise anatomical location.
... For the treatment of OCD in dystonia patients, Exposure and Response Prevention (ERP), a technique in which the patient is repeatedly exposed to situations that provoke the ritualistic behavior and instructed to resist performing them, may be tried. Although evidence is insufficient, a single case report showed ERP effective in treating OCD associated with dystonia secondary to basal ganglia infarction [61]. Minding the disabling nature of OCD and safety of ERP, this treatment should be trialed in the cases of comorbid OCD [8]. ...
... Of note, lesion studies also implicate OFC corticostriatal circuits in OCD pathology. ''Secondary OCD'' can result from lesions of the basal ganglia (Carmin et al., 2002), particularly in the head of the caudate (Chacko et al., 2000), or from infarct or injury to the left or right OFC (Kim and Lee, 2002;Ogai et al., 2005). Conversely, there are also striking cases in which patients with longstanding, intractable OCD have showed marked improvement in symptoms following basal ganglia hemeorrhage affecting the OFC-striatal circuit (Yaryura-Tobias and Neziroglu, 2003;Fujii et al., 2005). ...
Corticostriatal circuits through the orbitofrontal cortex (OFC) play key roles in complex human behaviors such as evaluation, affect regulation and reward-based decision-making. Importantly, the medial and lateral OFC (mOFC and lOFC) circuits have functionally and anatomically distinct connectivity profiles which differentially contribute to the various aspects of goal-directed behavior. OFC corticostriatal circuits have been consistently implicated across a wide range of psychiatric disorders, including major depressive disorder (MDD), obsessive compulsive disorder (OCD), and substance use disorders (SUDs). Furthermore, psychiatric disorders related to OFC corticostriatal dysfunction can be addressed via conventional and novel neurostimulatory techniques, including deep brain stimulation (DBS), electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS), and transcranial direct current stimulation (tDCS). Such techniques elicit changes in OFC corticostriatal activity, resulting in changes in clinical symptomatology. Here we review the available literature regarding how disturbances in mOFC and lOFC corticostriatal functioning may lead to psychiatric symptomatology in the aforementioned disorders, and how psychiatric treatments may exert their therapeutic effect by rectifying abnormal OFC corticostriatal activity. First, we review the role of OFC corticostriatal circuits in reward-guided learning, decision-making, affect regulation and reappraisal. Second, we discuss the role of OFC corticostriatal circuit dysfunction across a wide range of psychiatric disorders. Third, we review available evidence that the therapeutic mechanisms of various neuromodulation techniques may directly involve rectifying abnormal activity in mOFC and lOFC corticostriatal circuits. Finally, we examine the potential of future applications of therapeutic brain stimulation targeted at OFC circuitry; specifically, the role of OFC brain stimulation in the growing field of individually-tailored therapies and personalized medicine in psychiatry.
... Like TS, differences in striatal volume have been reported in patients with OCD [235][236][237] and fMRI studies have shown altered activities in the striatum, orbitofrontal cortex (OFC), and anterior cingulate (ACC) cortex during resting state and during the expression of symptoms 238,239 . OCD is most commonly treated with selective serotonin-reuptake inhibitors (SSRI) and cognitive behavioral therapy, and studies have shown decreased activity in the striatum and OFC following these treatments 232,240 . Recently, genetic animal models of OCD have been generated that exhibit both corticostriatal dysfunction, as well as a common dysfunction in glutamate signaling 232 . ...
The embryonic subpallium produces many different neuronal cell types present throughout the adult telencephalon, including striatal medium spiny neurons (MSN) and cortical interneurons. Dysfunction of either cell type leads to neurological and psychiatric disorders including schizophrenia, epilepsy, and Tourette’s syndrome. Thus, understanding the molecular pathways that regulate their development and function has important implications for understanding disease pathogenesis. This work describes novel methods and genetic factors that expand our ability to characterize the development and function of two major subpallial derivatives: cortical interneurons and striatal MSN. The first part of this thesis characterizes a novel enrichment method for producing parvalbumin-expressing (PV) interneurons from mouse embryonic stem cells. This method, which uses an atypical protein kinase C inhibitor to enhance intermediate neurogenesis, results in a markedly increased ratio of PV+ to somatostatin-expressing interneurons. The findings suggest that the mode of neurogenesis influences cortical interneuron fate determination. Moreover, PV+ interneurons can now be generated in large numbers to study their development, screen for factors that affect their physiology, and used in therapeutic applications. The second part of this thesis examines the function of two putative transcription factors, Zswim5 and Zswim6, in the regulation of striatal development. We show that these genes are expressed in subpallial precursors, and in the case of Zswim6, expressed in the adult striatum. Next, through the generation of Zswim5 and Zswim6 knockout mice, we provide a detailed anatomical, molecular, and behavioral characterization of the resulting phenotypes. Our findings reveal that loss of Zswim6 causes a reduction in striatal volume and morphological changes in MSN. Additionally, these structural changes are associated with alterations in motor behaviors including hyperactivity, impaired rotarod performance, and hyperresponsiveness to amphetamine. These results demonstrate that Zswim6 is indispensable for normal brain development and support findings in human genome-wide association studies that implicate Zswim6 with schizophrenia. Collectively, this dissertation provides novel insights into telencephalic development through the development of in vitro stem cell systems and in vivo disease mouse models that further our ability to test and understand neurological diseases.
... [24][25][26] Further OCD symptoms are reported damage to the basal ganglia, especially the caudate and orbitofrontal cortex. [27,28] Also, dysfunction of the basal ganglia secondary to a streptococcal infection [29] or encephalitis lethargic [30] has also been associated with the development of OCD. Although NSS are described as nonlocalizing neurological abnormalities, neuroimaging studies have suggested associations of NSS with activation changes in the sensorimotor cortex, supplementary motor area, cerebellum, basal ganglia, and thalamus. ...
Objective:
Modern research on obsessive-compulsive disorder (OCD) indicates that the primary cause of OCD, which was earlier explained only on basis of psychoanalytical theories, is biological. Our study attempts to investigate the neurobiological signs in form of soft neurological signs and cognitive function in OCD.
Methods:
A cross sectional study was conducted at psychiatric facility of Seth G.S. Medical College and KEM Hospital.
Materials and method:
50 OCD patients and age- and education-matched controls were selected for the study. Established instruments were used to assess the neurological soft signs (NSS) and the cognitive deficits.
Results:
OCD patients had significant more NSS in tests for motor coordination, sensory integration, complex motor tasks, hard signs, and right/left and spatial orientation. Cognitive deficits in the domains of visuospatial ability, executive function, attention, and working memory were significantly more in OCD patients compared to controls.
Conclusion:
Our study highlights the role of biological factors in form of soft neurological signs and cognitive dysfunction in the development of the OCD.
... No systematic studies connecting brain tumours or strokes to OCD were identified, however some case reports exist (e.g., Carmin et al., 2002;Kumar et al., 2009). ...
... These observations are complementary to those found in psychiatric research in which hypometabolism has been described in functional OCD (McGuire 1995). Therapies of poststroke OCD include medication, but cognitive behaviour therapy-in the form of exposure and response prevention-also seems to be potentially effective (Carmin et al. 2002). ...
The term 'behavioural' is often used in neurology to denote non-cognitive mental symptoms or disorders, thus including many psychiatric symptoms such as mood and psychotic disorders but also abnormal personality traits such as impulsivity and aggression or even social isolation. However, this chapter focuses on a more operational and restricted definition of this term. In psychology, the notion of behaviour includes the responses or reactions of an individual in front of a stimulus or in a given environment. The mechanisms by which brain lesions can affect a patient's behaviour depend on the pathogeny of lesions but also on their localization. In the acute case, altered perceptual and mental states can mimic confusional states and delusional symptoms. In the more chronic states, different deficits can modify behavioural response after stroke, and these causes correspond to the different steps that will lead to the patient's reaction.
... The second hypothesis is based on the existence of a pathophysiological substrate related to the basal ganglia described in functional imaging studies for both BS 1 and OCD 25,26 , supporting the classical interpretation of this co-existence as secondary to behavioral related cortico-striatal circuitry dysfunction. Reinforcing this hypothesis, obsessive-compulsive symptoms have been described after focal lesions involving the basal ganglia 27 , besides being part of the clinical expression of disorders classically related to pathological abnormalities of this brain region such as post-encephalitic parkinsonism, Gilles de la Tourette syndrome and pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection; Sydenham chorea and hereditary myoclonus-dyston i a 2 0 , 2 8 -3 0 . Similarly, Ya r y u r a -Tobias and Neziroglu 3 1 described the case of a patient with severe OCD that remitted following a unilateral basal ganglia hemo r r h a g e . ...
Background: Blepharospasm (BS) is a form of central focal dystonia recently associated with psychiatric disorders, particularly obsessive and compulsive symptoms. Hemifacial spasm (HFS) represents a focal myoclonus with peripheral origin in the facial nerve. Objective: To determine the frequency of obsessive and compulsive symptoms inpatients with BS in comparison with patients with HFS. Methods: 30 patients from each group (BS and HFS) followed by the botulinum toxin clinic at the HC-UFPR were evaluated using a structured interview based on the DSM-IV criteria and the Yale-Brown scale. Results:were compared by the mean two-tailed t test. Results:We found obsessive or compulsive symptoms in 20 (66.6%) patients with BE and 21 (70%) with HFS. Yale-Brown scale scores for each group were higher among BS patients; however, diferences were not statisticaly significant. Conclusion: Our study did not show a significant diference in the comparison of the prevalence of obsessive and compulsive symptoms among patients with BS and HFS.
... A number of studies have shown a strong correlation between several aspects of OCD and drug addiction. There is strong evidence in the literature that a hyperdopaminergic state plays an important role in the pathophysiology of both OCD and substance use disorders (Goodman et al., 1990;Mcdougle et al., 1994Mcdougle et al., , 2000Carmin et al., 2002; Bystritsky et al., 2004;Denys et al., 2004;Westenberg et al., 2007;Fontenelle et al., 2011). This hyperdopaminergic state can be modulated indirectly through antagonists of 5-HT3 receptors. ...
The aim of this study was to investigate the efficacy and safety of ondansetron as an augmentative agent to fluvoxamine in the treatment of patients with obsessive-compulsive disorder (OCD). Forty-six men and women, aged 18-60 years, who fulfilled the diagnostic criteria of OCD on the basis of the DSM-IV-TR and had a Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score of at least 21 were recruited into the study. The patients randomly received either ondansetron (8 mg/day) or placebo for 8 weeks. All patients received fluvoxamine (100 mg/day) for the first 4 weeks, followed by 200 mg/day for the rest of the trial. The patients were assessed using the Y-BOCS and the adverse event checklists at baseline, and the second, fourth, sixth, and eighth week. Forty-four patients completed the study. The Y-BOCS total score as well as the Y-BOCS obsession subscale score and compulsion subscale score showed significantly greater reduction in the ondansetron group than in the placebo group. There was no significant difference in adverse events between the two groups. In this 8-week double-blind randomized-controlled trial, ondansetron showed significant beneficial effect as an augmentative agent with fluvoxamine in patients with moderate to severe OCD and it was generally well tolerated.
... En este contexto se describen lesiones hemorrágicas e isquémicas, generalmente unilaterales en los ganglios basales; infartos orbitofrontales y talámicos; afectación de la arteria cerebral media, y lesiones hemisféricas y vasculopatías lenticuloestriadas de la infancia de aparición tardía, por mencionar las más importantes (49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59). ...
Introduction: Cerebrovascular disease is a major public health problem and common cause of neuropsychiatric disorders in the medically ill. Vascular lesions in the Central Nervous System cause signifi cant morbidity, usually followed by severe cognitive dysfunctions which become an important risk factor for developing psychopathology during the course of cerebrovascular disorders. Objective: To describe neuropsychiatric disorders affecting people with stroke other than post-stroke depression, as this will be reviewed extensively elsewhere. Method: Review of medical literature. Conclusions: Research on the neurobiology of mental disorders based on vascular theories to explain the etiology and physiopathology of some mental disorders has not come up with consistent results linking structural and functional studies with clinical correlates of neuropsychiatric syndromes. Implicit mechanisms responsible for the blend between systemic disease, neurological disorders and psychiatry are still poorly understood by the scientifi c community responsible for the treatment of cerebrovascular patients. Most studies are limited to case reports and series in severely ill patients leaving out those patients with mild to moderate stroke. These subjects are known to be at risk for neuropsychiatric disorders involving movement and cognitive symptoms such as Parkinson’s, dementia and delirium.
... Lastly, some older adults might experience OCD symptoms for the first time in late life. Late-onset OCD was associated with several neurological disorders in some reports (e.g., Carmin & Wiegartz, 2000;Carmin, Wiegartz, Yunus, & Gillock, 2002;Scicutella, 2000). Nestadt, Bienvenu, Cai, Samuels, and Eaton (1998) evaluated the age at onset of OCD in a follow-up evaluation of the Baltimore Epidemiologic Catchment Area Study. ...
Although obsessive-compulsive disorder (OCD) has received increasing attention, the study and treatment of OCD in late life has been neglected. The obsessions and compulsions seen with older adults do not appear to differ from the symptoms experienced by other age groups, although developmental issues might influence symptom focus (e.g., memory functioning-related obsessions). Hoarding difficulties might be prevalent in late life, although additional studies are needed. Seniors with OCD can present with comorbid psychiatric disorders, multiple general medical problems, and impaired cognitive functioning, complicating evaluation. There have not been controlled clinical trials of cognitive-behavioral therapy (CBT) for late-life OCD, although initial reports suggest older adults respond to CBT that includes age-related treatment modifications. We illustrate the challenges to assessing and treating older adults with OCD with case examples involving memory-related obsessions and clinical hoarding. The successful strategies used for adapting CBT for the treatment of late-life generalized anxiety disorder might serve as a model for advancing the study and treatment of late-life OCD.
... En este contexto se describen lesiones hemorrágicas e isquémicas, generalmente unilaterales en los ganglios basales; infartos orbitofrontales y talámicos; afectación de la arteria cerebral media, y lesiones hemisféricas y vasculopatías lenticuloestriadas de la infancia de aparición tardía, por mencionar las más importantes (49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59). ...
Introduction: Cerebrovascular disease is a major public health problem and common cause of neuropsychiatric disorders in the medically ill. Vascular lesions in the Central Nervous System cause signifi cant morbidity, usually followed by severe cognitive dysfunctions which become an important risk factor for developing psychopathology during the course of ce- rebrovascular disorders. Objective: To describe neuropsychiatric disorders affecting people with stroke other than post-stroke depression, as this will be reviewed extensively elsewhere. Method: Review of medical literature. Conclusions: Research on the neurobiology of mental disorders based on vascular theories to explain the etiology and physiopathology of some mental disorders has not come up with consistent results linking structural and functional
... Elderly individuals may be at higher risk for developing OCD because of their proneness to stroke-related neuropsychiatric disorders. Several reports suggested that late-onset OCD is frequently associated with organic brain diseases, including stroke, transient ischemic attack, and organophosphate poisoning [2][3][4] The common comorbidities associated with OCD include major depression, tic disorder, psychotic disorder, and impulse-control disorders; however, concurrent or longitudinal overlaps of narcolepsy within both functional and organic causes of OCD have not been reported in medical literature as yet, as shown from an extensive search on MEDLINE and PubMed. ...
Understanding the function of glutamate transporters has broad implications for explaining how neurons integrate information and relay it through complex neuronal circuits. Most of what is currently known about glutamate transporters, specifically their ability to maintain glutamate homeostasis and limit glutamate diffusion away from the synaptic cleft, is based on studies of glial glutamate transporters. By contrast, little is known about the functional implications of neuronal glutamate transporters. The neuronal glutamate transporter EAAC1 is widely expressed throughout the brain, particularly in the striatum, the primary input nucleus of the basal ganglia, a region implicated with movement execution and reward. Here, we show that EAAC1 limits synaptic excitation onto a population of striatal medium spiny neurons identified for their expression of D1 dopamine receptors (D1-MSNs). In these cells, EAAC1 also contributes to strengthen lateral inhibition from other D1-MSNs. Together, these effects contribute to reduce the gain of the input-output relationship and increase the offset at increasing levels of synaptic inhibition in D1-MSNs. By reducing the sensitivity and dynamic range of action potential firing in D1-MSNs, EAAC1 limits the propensity of mice to rapidly switch between behaviors associated with different reward probabilities. Together, these findings shed light on some important molecular and cellular mechanisms implicated with behavior flexibility in mice.
Understanding the function of glutamate transporters has broad implications for explaining how neurons integrate information and relay it through complex neuronal circuits. Most of what is currently known about glutamate transporters, specifically their ability to maintain glutamate homeostasis and limit glutamate diffusion away from the synaptic cleft, is based on studies of glial glutamate transporters. By contrast, little is known about the functional implications of neuronal glutamate transporters. The neuronal glutamate transporter EAAC1 is widely expressed throughout the brain, particularly in the striatum, the primary input nucleus of the basal ganglia, a region implicated with movement execution and reward. Here, we show that EAAC1 limits synaptic excitation onto a population of striatal medium spiny neurons identified for their expression of D1 dopamine receptors (D1-MSNs). In these cells, EAAC1 also contributes to strengthen lateral inhibition from other D1-MSNs. Together, these effects contribute to reduce the gain of the input-output relationship and increase the offset at increasing levels of synaptic inhibition in D1-MSNs. By reducing the sensitivity and dynamic range of action potential firing in D1-MSNs, EAAC1 limits the propensity of mice to rapidly switch between behaviors associated with different reward probabilities. Together, these findings shed light on some important molecular and cellular mechanisms implicated with behavior flexibility in mice.
Understanding the function of glutamate transporters has broad implications for explaining how neurons integrate information and relay it through complex neuronal circuits. Most of what is currently known about glutamate transporters, specifically their ability to maintain glutamate homeostasis and limit glutamate diffusion away from the synaptic cleft, is based on studies of glial glutamate transporters. By contrast, little is known about the functional implications of neuronal glutamate transporters. The neuronal glutamate transporter EAAC1 is widely expressed throughout the brain, particularly in the striatum, the primary input nucleus of the basal ganglia, a region implicated with movement execution and reward. Here, we show that EAAC1 limits synaptic excitation onto a population of striatal medium spiny neurons identified for their expression of D1 dopamine receptors (D1-MSNs). In these cells, EAAC1 also contributes to strengthen lateral inhibition from other D1-MSNs. Together, these effects contribute to reduce the gain of the input-output relationship and increase the offset at increasing levels of synaptic inhibition in D1-MSNs. By reducing the sensitivity and dynamic range of action potential firing in D1-MSNs, EAAC1 limits the propensity of mice to rapidly switch between behaviors associated with different reward probabilities. Together, these findings shed light on some important molecular and cellular mechanisms implicated with behavior flexibility in mice.
Understanding the function of glutamate transporters has broad implications for explaining how neurons integrate information and relay it through complex neuronal circuits. Most of what is currently known about glutamate transporters, specifically their ability to maintain glutamate homeostasis and limit glutamate diffusion away from the synaptic cleft, is based on studies of glial glutamate transporters. By contrast, little is known about the functional implications of neuronal glutamate transporters. The neuronal glutamate transporter EAAC1 is widely expressed throughout the brain, particularly in the striatum, the primary input nucleus of the basal ganglia, a region implicated with movement execution and reward. Here, we show that EAAC1 limits synaptic excitation onto a population of striatal medium spiny neurons identified for their expression of D1 dopamine receptors (D1-MSNs). In these cells, EAAC1 also contributes to strengthen lateral inhibition from other D1-MSNs. Together, these effects contribute to reduce the gain of the input-output relationship and increase the offset at increasing levels of synaptic inhibition in D1-MSNs. By reducing the sensitivity and dynamic range of action potential firing in D1-MSNs, EAAC1 limits the propensity of mice to rapidly switch between behaviors associated with different reward probabilities. Together, these findings shed light on some important molecular and cellular mechanisms implicated with behavior flexibility in mice.
The two forms of obsessive-compulsive disorder (OCD), idiopathic and acquired, have been linked to abnormalities in the fronto-striato-thalamo-cortical circuitry, involving the orbitofrontal cortex, anterior cingulate cortex, thalamus, and striatum. Accumulating evidence indicates that damage to other brain regions (ie, temporal lobes) is also implicated in the pathogenesis of both types of OCD. In addition, some discrete OCD symptoms have received less attention because of their presumed low occurrence and difficultly of categorization. Among these, one intriguing and potentially severe type of obsessive thinking is the so-called "need to know" (NtK), which is a strong urge to access certain information, particularly proper names. In some patients, this monosymptomatic presentation may constitute the major feature of OCD. Here we report the cases of two patients who developed NtK obsessions with tenacious time-consuming, answer-seeking compulsions as the only or more disabling symptomatology in association with malignant tumors involving the right temporal lobe and connected fronto-subcortical circuits.
Background: Cases of obsessive-compulsive disorder (OCD) following cerebrovascular accident (CVA) have rarely been reported. Methods: Case report and literature review. Results: We describe the case of a 58-year-old, right-handed man developed OCD 17 months after stroke resulting from lesion of the right middle cerebral artery infarction. The patient was successfully treated with sertraline up to 50 mg per day. His OCD behaviors largely reduced in 6 weeks, and the Yale-Brown Obsessive Compulsive Scale score was reduced from 29 to 12 in 1 year. A literature review revealed 21 previous cases of OCD following CVA. Among these, consistent with our case, the basal ganglia was the most common site of the lesion responsible for the development of this rare disorder. We discuss the patient's treatment and outcomes. Conclusions: Our present case and a literature review suggest that OCD can manifest following CVA, although further studies are necessary. Selective serotonin reuptake inhibitors appear to be effective in treating this rare disorder.
A Transdiagnostic Approach to Obsessions, Compulsions and Related Phenomena - edited by Leonardo F. Fontenelle January 2019
Obsessive-compulsive disorder (OCD) is a clinical syndrome characterised by recurrent intrusive thoughts (obsessions) and repetitive mental or behavioural acts (compulsions), typically performed in response to obsessions or related anxiety. OCD generally has a stable symptom pattern throughout life but nevertheless is well known for its heterogeneity, as symptomatic presentations and comorbidity patterns differ widely among patients. A number of other psychiatric and neurological disorders may share similar phenomenological characteristics with OCD or are sometimes conceptualised as atypical OCDs. These heterogeneous aspects of the disorder have led to a search for OCD subtypes that might be associated with different aetiologies or treatment responses.
Obsessive-compulsive disorder (OCD) is present in 1.5-2.5% of the population and can result in substantial lifelong disability. It is characterized by intrusive thoughts, sensations, and urges and by repetitive behaviors that are difficult to control despite, in most cases, preserved insight as to their excessive or irrational nature. The causes and underlying pathophysiology of OCD are not well understood, which has limited the development of new treatments and interventions. Despite evidence for a substantial genetic contribution to disease risk, identification and replication of genetic variants associated with OCD have been challenging. Decades of candidate gene association studies have provided little insight. They are now being supplanted by modern genomewide approaches to discover both common and rare sequence and structural variants. Studies to date suggest potential novel therapeutic avenues such as modulators of glutamatergic and immune pathways; however, individual genetic findings are not yet statistically robust or replicated. Further efforts are clearly needed to identify specific risk variants and to confirm vulnerable pathways by studying much larger cohorts of patients with comprehensive variant discovery approaches. Mouse knockout models have already made notable inroads into our understanding of OCD pathology; their utility will only increase as specific risk alleles are identified.
Obsessive-compulsive disorder (OCD) and related conditions significantly diminish quality of life and are most disabling for affected older adults. We review the phenomenology, epidemiology, assessment, and treatment of older adults’ experience of OCD and the related, although importantly distinct condition, Hoarding Disorder (HD). Late-life OCD remains significantly understudied possibly because of low prevalence estimates in some studies. Studies of HD prevalence indicate older adults’ more often experience the disorder, which appears to increase in severity over the life span. Psychometric studies of psychological measures of OCD and OCD-related disorders with older adult samples are lacking, which has made research and clinical assessment more difficult. There have not been controlled clinical trials of treatments for late-life OCD or OCD-related disorders. Developmental stage adjusted applications of empirically supported psychosocial treatments, when combined with structured cognitive rehabilitation procedures, have significantly reduced HD symptoms. The rapid aging of the population and the debilitating nature of late-life OCD and related problems should make accelerated study of these disorders a public health priority.
OCD is the fourth most common neuropsychiatric disorder with lifetime prevalence estimates of 0.4?3.5%. Family and twin studies suggest a strong genetic component, and molecular genetic studies are being carried out to identify genes contributing risk to OCD. It is postulated as a frontal-striatal disorder and functional neuroimaging studies provide a strong support for the dysfunction of cortico-striatal-thalamic-cortical neurocircuit. OCD can be secondary to a variety of medical conditions that range from deteriorative neurological illness, to head injury, and to autoimmune disorders. Few reports and no controlled studies exist in the treatment of acquired/secondary OCD. Both CBT and pharmacotherapy are effective first-line treatment modalities for OCD. Brain stimulation and/or psychosurgery have been tried with varying success in treatment of refractory OCD. Environmental, genetic, and clinical factors interact in a complex fashion in the individual patient. This chapter will examine OCD from the medical perspective.
Structural brain lesions can be a rare cause of refractory psychiatric symptoms. The analysis of such cases may lead to insights into psychiatric neurobiology. Here we present a case of a dronabinol-responsive obsessive-compulsive syndrome after thalamic infarct.
Obsessive-compulsive disorder (OCD) is a common form of neurosis. Symptoms of OCD could develop as a sign of focal brain lesion, particularly in multiple sclerosis, extrapyramidal disorders, epilepsy, less frequently — in other diseases. Timely diagnosis and treatment of the symptoms of OCD is an important aspect in the management of mentioned neurological disorders.
Obsessive–compulsive disorder is a common disorder. Clinically, the disorder is characterized by significant symptom differences across patients. This review discusses the current diagnostic status, symptom presentation, common measurement tools, dominant biological and psychological models, and the most common treatment approaches for this disorder.
Obsessive-compulsive disorder with verification or washing rituals, for example, can be extremely debilitating and in 10 % of cases do not respond to psychotherapy or medication. Highly focused surgical procedures have been proposed, in particular lesions in the internal capsule and the cingulum to interrupt loops causing this disorder. These relatively effective interventions, capsulotomy, or cingulotomy, are however irreversible, and can make some definitive complications. With the advent of deep brain stimulation targets such as the internal capsule were taken and others, such as the subthalamic nucleus accumbens, came to be added. This stimulation through electrodes implanted in the brain has the advantage of being reversible and adaptable.
Les troubles obsessionnels compulsifs,avec par exemple leurs rituels de vérification ou de lavage, peuvent devenir extrêmement invalidants, et dans 10 % des cas ne répondre à aucune psychothérapie ni traitement médicamenteux. Des gestes chirurgicaux très focalisés ont été proposés consistant notamment en des lésions au niveau de la capsule interne ou du cingulum, afin d’interrompre les boucles à l’origine de ces troubles. Ces interventions, de capsulotomie ou de cingulotomie, relativement efficaces, présentent néanmoins l’inconvénient d’être irréversibles, et peuvent rendre certaines complications définitives. Avec l’avènement de la stimulation cérébrale profonde, des cibles comme la capsule interne ont été reprises et d’autres, telles que les noyaux sous-thalamique ou accumbens, sont venues s’y ajouter. Cette stimulation, par des électrodes implantées dans le cerveau, possède l’avantage d’être réversible et adaptable.
IntroductionDetecting OCDClinical assessment of obsessive-compulsive symptomsInsightAssessment of the risk of suicideDifferential diagnosis, comorbidities and related disordersConclusions
References
Anxiety is present in at least 20 % of stroke patients already in the acute phase and once present tends to run a chronic course. Of the different anxiety disorders, generalized anxiety disorder is the most common. The concept of “post-stroke anxiety,” as a direct consequence of biological mechanisms associated to stroke is controversial. More likely, the etiology of anxiety after stroke is probably multifactorial, associated with, e.g., personality traits, psychosocial stressors, and yet unknown biological mechanisms. The role of the stroke lesion location is unknown, although posterior right hemisphere location has been suggested in generalized anxiety, right temporal location in panic disorder, and lesions affecting the frontal-subcortical circuitry in the obsessive-compulsive disorder (OCD). Compared to post-stroke depression, anxiety has been far less studied. Yet it has a strong negative impact on the quality of life of the stroke victims and their caregivers, and it is associated with impaired activities of daily living and probably also premature institutionalization. Although the validity of structured methods and rating scales is probably suboptimal, their routine use is recommended to improve detection of this often neglected disorder. There are no randomized controlled high-quality studies of the management or pharmaceutical treatment. In clinical practice most of the patients seem to benefit from the serotonin-selective reuptake inhibitors and other antianxiety drugs that are widely used in general psychiatry. However, neuroleptics, benzodiazepines, and tricyclic antidepressants should be used with caution in this fragile patient population.
Literature evidence suggests that onset of obsessive-compulsive disorder (OCD) at a later age is usually associated with brain lesions. However, none of previous reports suggest an association between arachnoid cyst and OCD. In this report, we present a case of OCD, starting at the age of 40 years, in which the obsessive symptoms were characteristically associated with fluctuating insight. Investigation revealed an arachnoid cyst, in the area of left fronto-parietal region, with broad base towards the falx.
Deep brain stimulation was first developed for movement disorders but is now being offered as a therapeutic alternative in severe psychiatric disorders after the failure of conventional therapies. One of such pathologies is obsessive-compulsive disorder. This disorder which associates intrusive thoughts (obsessions) and repetitive irrepressible rituals (compulsions) is characterized by a dysfunction of a cortico-subcortical loop. After having reviewed the pathophysiological evidence to show why deep brain stimulation was an interesting path to take for severe and resistant cases of obsessive-compulsive disorder, we will present the results of the different clinical trials. Finally, we will provide possible mechanisms for the effects of deep brain stimulation in this pathology.
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This case study demonstrates an effective course of exposure/response prevention (EX/RP) in an 82-year-old man with late-onset obsessive-compulsive disorder (OCD) with no apparent neurobiological changes. The results indicated significant reductions in time spent on rituals, anxiety associated with obsessions, and depression. Treatment gains were maintained and continued to progress through appropriate aftercare. In this case, a graduate student therapist learned and applied EX/RP after engaging in a training process. Results highlight the importance of life stressors in the development of OCD and that EX/RP can be applied to older adults with certain modifications. The results are promising for the implementation of EX/RP in older adults with OCD; however, future randomized controlled trials are needed.
This article reviews the literature on obsessive-compulsive disorders with the objective of discussing the current state of the scientific research on this topic. The authors refer to the international literature and stress Brazilian research, especially that carried out by their own group, PROTOC (Obsessive-Compulsive Spectrum Disorders Project).
Treatment efficacy of Deep Brain Stimulation (DBS) and other neurosurgical techniques in refractory Obsessive-Compulsive Disorder (OCD) is greatly dependent on the targeting of relevant brain regions. Over the years, several case reports have been published on either the emergence or resolution of obsessive-compulsive symptoms due to neurological lesions. These reports can potentially serve as an important source of insight into the neuroanatomy of compulsivity and have implications for targets of DBS. For this purpose, we have reviewed all published case reports of patients with acquired or resolved obsessive-compulsive symptoms after brain lesions. We found a total of 37 case reports describing 71 patients with acquired and 6 with resolved obsessive-compulsive symptoms as a result of hemorrhaging, infarctions or removal of tumors. Behavioral symptoms following brain lesions consisted of typical obsessive-compulsive symptoms, but also symptoms within the compulsivity spectrum. These data suggests that lesions in the cortico-striato-thalamic circuit, parietal and temporal cortex, cerebellum and brainstem may induce compulsivity. Moreover, the resolution of obsessive-compulsive symptoms has been reported following lesions in the putamen, internal capsule and fronto-parietal lobe. These case reports provide strong evidence supporting the rationale for DBS in the ventral striatum and internal capsule for treatment of compulsivity and reveal the putamen and fronto-parietal cortex as promising new targets.
This report presents a syndrome resembling obsessive convulsive disorder (OCD) secondary to a stroke in the left basal ganglia. The patient's syndrome is virtually identical to those that have been described in bilateral damage of the basal ganglia. However, the stroke described in this case report is located unilaterally in the left basal ganglia. In addition, experience in treating a patient with OCD induced by structural damage of basal ganglia is presented.
Assessed the efficacy of an established behavioral treatment for obsessive compulsive disorder (OCD) administered to an elderly sample in a clinical setting. Ss were 11 elderly OCD inpatients (mean age 68.7 yrs) and 11 younger OCD inpatients (mean age 30.3 yrs) in a behavioral medicine unit. Ss underwent individualized treatment that featured exposure and response prevention. At discharge, Ss rated the extent of improvement they had experienced in each of the primary symptoms of OCD on an 11-point goal attainment scale. In addition, Ss were rated as responders of nonresponders. There was no significant difference in improvement ratings between the 2 groups at the time of discharge. Both mean ratings were in the range designated as significant improvement. 72% of the elderly Ss and 63% of the younger Ss were classified as treatment responders. Results indicate that older patients can benefit from cognitive behavioral treatment for OCD and that the level of improvement experienced may be comparable to that of younger adults. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The development of a 21-item self-report inventory for measuring the severity of anxiety in psychiatric populations is described. The initial item pool of 86 items was drawn from three preexisting scales: the Anxiety Checklist, the Physician’s Desk Reference Checklist, and the Situational Anxiety Checklist. A series of analyses was used to reduce the item pool. The resulting Beck Anxiety Inventory (BAI) is a 21-item scale that showed high internal consistency (α = .92) and test—retest reliability over 1 week, r (81) = .75. The BAI discriminated anxious diagnostic groups (panic disorder, generalized anxiety disorder, etc.) from nonanxious diagnostic groups (major depression, dysthymic disorder, etc). In addition, the BAI was moderately correlated with the revised Hamilton Anxiety Rating Scale, r (150) = .51, and was only mildly correlated with the revised Hamilton Depression Rating Scale, r (153) = .25.
Four cases of obsessive-compulsive disorder arising in late life in association with a presumed organic aetiology are described. Three of the four had brief episodes of OCD earlier in their lives. Neuropsychological assessment demonstrated impairments in verbal fluency and visuo-spatial tasks. No case exhibited global intellectual impairment. The two patients who complied with appropriate treatment became asymptomatic after 4-6 months.
The difficulties inherent in obtaining consistent and adequate diagnoses for the purposes of research and therapy have been pointed out by a number of authors. Pasamanick12 in a recent article viewed the low interclinician agreement on diagnosis as an indictment of the present state of psychiatry and called for "the development of objective, measurable and verifiable criteria of classification based not on personal or parochial considerations, but on behavioral and other objectively measurable manifestations."Attempts by other investigators to subject clinical observations and judgments to objective measurement have resulted in a wide variety of psychiatric rating scales.4,15 These have been well summarized in a review article by Lorr11 on "Rating Scales and Check Lists for the Evaluation of Psychopathology." In the area of psychological testing, a variety of paper-and-pencil tests have been devised for the purpose of measuring specific
• The development design and reliability of the Yale-Brown Obsessive Compulsive Scale have been described elsewhere. We focused on the validity of the Yale-Brown Scale and its sensitivity to change. Convergent and discriminant validity were examined in baseline ratings from three cohorts of patients with obsessive-compulsive disorder (N = 81). The total Yale-Brown Scale score was significantly correlated with two of three independent measures of obsessive-compulsive disorder and weakly correlated with measures of depression and of anxiety in patients with obsessive-compulsive disorder with minimal secondary depressive symptoms. Results from a previously reported placebo-controlled trial of fluvoxamine in 42 patients with obsessive-compulsive disorder showed that the Yale-Brown Scale was sensitive to drug-induced changes and that reductions in Yale-Brown Scale scores specifically reflected improvement in obsessive-compulsive disorder symptoms. Together, these studies indicate that the 10-item Yale-Brown Scale is a reliable and valid instrument for assessing obsessive-compulsive disorder symptom severity and that it is suitable as an outcome measure in drug trials of obsessive-compulsive disorder.
• The Yale-Brown Obsessive Compulsive Scale was designed to remedy the problems of existing rating scales by providing a specific measure of the severity of symptoms of obsessivecompulsive disorder that is not influenced by the type of obsessions or compulsions present. The scale is a clinician-rated, 10-item scale, each item rated from 0 (no symptoms) to 4 (extreme symptoms) (total range, 0 to 40), with separate subtotals for severity of obsessions and compulsions. In a study involving four raters and 40 patients with obsessive-compulsive disorder at various stages of treatment, interrater reliability for the total Yale-Brown Scale score and each of the 10 individual items was excellent, with a high degree of internal consistency among all item scores demonstrated with Cronbach's α coefficient. Based on pretreatment assessment of 42 patients with obsessive-compulsive disorder, each item was frequently endorsed and measured across a range of severity. These findings suggest that the Yale-Brown Scale is a reliable instrument for measuring the severity of illness in patients with obsessive-compulsive disorder with a range of severity and types of obsessive-compulsive symptoms.
This report presents a syndrome resembling obsessive convulsive disorder (OCD) secondary to a stroke in the left basal ganglia. The patient's syndrome is virtually identical to those that have been described in bilateral damage of the basal ganglia. However, the stroke described in this case report is located unilaterally in the left basal ganglia. In addition, experience in treating a patient with OCD induced by structural damage of basal ganglia is presented.
Despite substantial evidence supporting the general efficacy of cognitive behavioral treatment for obsessive-compulsive disorder (OCD), little has been written to guide practitioners treating older adults with this potentially disabling condition. The present article reviews the research literature on the cognitive behavioral treatment of elders with OCD and discusses adaptations of treatment that may be required to respond effectively to clinical issues and challenges associated with this disorder in later life. Though more research is clearly needed, preliminary findings suggest exposure and response prevention is effective with older adults. However, practitioners may need to adjust clinical procedure to address medical comorbidity and physical and cognitive limitations associated with aging, cultural issues and attitudes that may promote treatment resistance and nonadherence, the influence of family members and other caretakers, and complications presented by stressors and fears common in older adults.
Prevalence rates (six month and lifetime) for a random sample (N=358) of the eldery living at home, are compared to the rates for a sample (N=3,258) of the whole adult popultion of Edmonton and found to be generally lower in the elderly, except for cognitive impairment. These household resident results are similar to those reported from the United States using similar methods. A sample (N = 199) of the elderly living in institutions was found to have a very high overall prevalence of illness, mostly consisting of cognitive impairment (69%). It is estimated that over half of all cases of cognitive impairment live in institutions. This has considerable implications for the programs in institutions for the elderly, and also the need for institutions in the future, unless alternate means of care can be developed.
3258 randomly selected adult household residents of Edmonton were interviewed by trained lay interviewers using the Diagnostic Interview Schedule (DIS). One of the diagnostic categories studied was obsessive-compulsive disorder (OCD). The lifetime and six month prevalence rates of OCD were 2.9% and 1.6% respectively. The morbidity risk, was equal in males and females at 5.4%. The peak age of risk of onset for both sexes was from the ages of 10 to 19 and, closely followed by the decade 20–29. Obsessions were found to be more frequently experienced than compulsions. Having a lifetime diagnosis of OCD is associated with an increased likelihood of developing depression, alcohol abuse, drug abuse, phobic disorders, and antisocial personality disorder. The significance of these findings is discussed for clinical practice.
The present report describes the development of the Penn State Worry Questionnaire to measure the trait of worry. The 16-item instrument emerged from factor analysis of a large number of items and was found to possess high internal consistency and good test-retest reliability. The questionnaire correlates predictably with several psychological measures reasonably related to worry, and does not correlate with other measures more remote to the construct. Responses to the questionnaire are not influenced by social desirability. The measure was found to significantly discriminate college samples (a) who met all, some, or none of the DSM-III-R diagnostic criteria for generalized anxiety disorder and (b) who met criteria for GAD vs posttraumatic stress disorder. Among 34 GAD-diagnosed clinical subjects, the worry questionnaire was found not to correlate with other measures of anxiety or depression, indicating that it is tapping an independent construct with severely anxious individuals, and coping desensitization plus cognitive therapy was found to produce significantly greater reductions in the measure than did a nondirective therapy condition.
Moral or religious scrupulosity is a disabling condition which is sometimes seen in patients with obsessive compulsive disorder (OCD). The authors described 10 patients with moral or religious scrupulosity who were treated with fluoxetine or clomipramine. Seven of the 10 patients completed open treatment of at least 8 weeks without requiring adjunctive medication; 5 of those 7 patients were rated as much improved. Among the 3 patients who required adjunctive medication, 1 was rated as much improved. Of the 4 nonresponders at 3 months, 2 responded after longer treatment trials. These results suggest that extreme moral or religious concerns and behaviors might be a form of OCD and that the scrupulosity can be effectively treated with serotonin reuptake blockers.
The development design and reliability of the Yale-Brown Obsessive Compulsive Scale have been described elsewhere. We focused on the validity of the Yale-Brown Scale and its sensitivity to change. Convergent and discriminant validity were examined in baseline ratings from three cohorts of patients with obsessive-compulsive disorder (N = 81). The total Yale-Brown Scale score was significantly correlated with two of three independent measures of obsessive-compulsive disorder and weakly correlated with measures of depression and of anxiety in patients with obsessive-compulsive disorder with minimal secondary depressive symptoms. Results from a previously reported placebo-controlled trial of fluvoxamine in 42 patients with obsessive-compulsive disorder showed that the Yale-Brown Scale was sensitive to drug-induced changes and that reductions in Yale-Brown Scale scores specifically reflected improvement in obsessive-compulsive disorder symptoms. Together, these studies indicate that the 10-item Yale-Brown Scale is a reliable and valid instrument for assessing obsessive-compulsive disorder symptom severity and that it is suitable as an outcome measure in drug trials of obsessive-compulsive disorder.
The Yale-Brown Obsessive Compulsive Scale was designed to remedy the problems of existing rating scales by providing a specific measure of the severity of symptoms of obsessive-compulsive disorder that is not influenced by the type of obsessions or compulsions present. The scale is a clinician-rated, 10-item scale, each item rated from 0 (no symptoms) to 4 (extreme symptoms) (total range, 0 to 40), with separate subtotals for severity of obsessions and compulsions. In a study involving four raters and 40 patients with obsessive-compulsive disorder at various stages of treatment, interrater reliability for the total Yale-Brown Scale score and each of the 10 individual items was excellent, with a high degree of internal consistency among all item scores demonstrated with Cronbach's alpha coefficient. Based on pretreatment assessment of 42 patients with obsessive-compulsive disorder, each item was frequently endorsed and measured across a range of severity. These findings suggest that the Yale-Brown Scale is a reliable instrument for measuring the severity of illness in patients with obsessive-compulsive disorder with a range of severity and types of obsessive-compulsive symptoms.
3,258 randomly selected adult household residents of Edmonton were interviewed by trained lay interviewers using the Diagnostic Interview Schedule (DIS). Six-month prevalence figures for DIS/DSM III diagnoses are given, and selected figures for the one-month and one-year prevalence, and the one-year symptom-free rates. The six-month prevalence for any diagnosis is 17.1%, comparable to findings from other population studies using DSM III derived diagnoses, but lower than studies using the PSE. The prevalence rates for most disorders tended to be lowest in the elderly, but this was not as marked as the drop in lifetime prevalence. Men had higher prevalence for substance use disorders than women, but women had higher rates for affective disorders and anxiety/somatoform disorders. Prevalences for all disorders were either similar or lower in those who were married or living as though married, than in those who were not cohabiting. One-year symptom-free rates were highest for those with substance use disorders and lowest for those with anxiety/somatoform disorders - largely due to the persistence of phobias.
A 71-year-old man with no previous psychiatric history presented with an acute onset of obsessive-compulsive disorder (OCD) symptoms associated with a right inferior parietal infarct. There were no abnormal neurological signs. There were no noteworthy abnormalities on neuropsychological testing.
Whereas a computerised tomography scan showed only a right inferior parietal infarct, a single photon emission computerised tomography (SPECT) scan revealed that in addition to the infarct there was decreased regional cerebral blood flow in the right basal ganglia and temporal areas. There was higher activity in the right orbitofrontal area than in the left.
The patient improved with standard drug therapy and psychotherapy.
SPECT is effective in the diagnosis of neuropsychiatric disorders such as OCD, and the pathological changes in brain metabolism detected by SPECT may be reversed by both drug therapy and psychotherapy.
Obsessive compulsive disorder (OCD) is a prevalent form of psychopathology in the elderly, yet limited evaluation of the disorder in this age group has occurred. We review the literature and describe a case of OCD effectively treated in an 80-year-old man. Case study reports suggest that elderly persons are responsive to selective serotonin uptake inhibitors, although medication selection and dosage may need to be adjusted as a result of the medical conditions sometimes present in the elderly. Elderly persons appear able to benefit from exposure and response prevention, although behavioral intervention has not been frequently used. We describe here the first case report where exposure and response prevention procedures were successfully used and this intervention was not confounded with psychopharmacologic treatment.
Elderly patients have a higher prevalence of clinically significant anxiety than younger patients. The anxiety is usually comorbid with depression, medical illness, dementia, or personality disorders, and all of these factors impact on treatment. Further complicating treatment are age-related changes in the pharmacokinetics and pharmacodynamics of anxiolytics in this patient population. Benzodiazepines, buspirone, beta-blockers, antidepressants, neuroleptics, and antihistamines are useful in treating anxiety in older patients, but individual patient physiologic and psychological characteristics need to be considered in choosing an appropriate agent.
The author reviewed the epidemiology and comorbidity of anxiety disorders in the elderly.
Data from 1970 onward were obtained through a computerized literature search, a review of Index Medicus, and the bibliographies of retrieved articles. Eight random-sample community surveys of anxiety disorders in persons 60 years of age or older were identified. Studies relating to the comorbidity of late-life anxiety and depression, dementia, alcoholism, and medical illness were also reviewed.
The majority of studies showed that anxiety disorders are less common in the elderly than in younger adults. Generalized anxiety disorder and phobias account for most anxiety in late life; panic disorder is rare. Agoraphobia, and possibly obsessive-compulsive disorder in females, may occur as a primary disorder for the first time in old age, whereas simple phobia, obsessive-compulsive disorder in males, and panic disorder either persist from younger years or arise in the context of another psychiatric or medical disorder. There is considerable comorbidity of geriatric depression and generalized anxiety disorder and phobias, although the depression usually goes untreated or is inappropriately treated with benzodiazepines. The rate of comorbidity of anxiety and medical illness and alcoholism is lower in the elderly than in younger persons.
Epidemiologic data on the prevalence of posttraumatic stress disorder (PTSD) and the first occurrence of generalized anxiety disorder and PTSD in late life are still needed. Further comorbidity studies are needed to determine the extent to which anxiety arises secondary to depression, as well as the optimal treatment and prognosis for this mixed state.
3258 randomly selected adult household residents of Edmonton were interviewed by trained lay interviewers using the Diagnostic Interview Schedule (DIS). One of the diagnostic categories studied was obsessive-compulsive disorder (OCD). The lifetime and six month prevalence rates of OCD were 2.9% and 1.6% respectively. The morbidity risk, was equal in males and females at 5.4%. The peak age of risk of onset for both sexes was from the ages of 10 to 19 and, closely followed by the decade 20-29. Obsessions were found to be more frequently experienced than compulsions. Having a lifetime diagnosis of OCD is associated with an increased likelihood of developing depression, alcohol abuse, drug abuse, phobic disorders, and antisocial personality disorder. The significance of these findings is discussed for clinical practice.
Anxiety disorders in-terview schedule for DSM-IV. Phobia and Anxiety Disorders Clinic, Center for Stress and Anxiety Treatment of obsessive compulsive disorder in the elderly: a review and case example
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Mental state examination for organic mental syn-drome in the elderly patient Geriatric psychiatry Develop-ment and validation of the Penn State Worry Questionnaire
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