OBSESSIVE_COMPULISVE_DISORDER_(OCD).pptx

OCD is psychiatric disorder that needs long term follow up and care for the patient and even his /her care givers... in sever cases it is considered a disabling disorder .

1. Obsessive Compulsive Disorder (OCD) By Dr. Ashraf Saad Elshazly MBBch , Msc ,M.D. KCMH

2. Learning Objectives To learn :- Epidemiology Etiology Clinical presentations Comorbidity Course of illness Treatment ( pharmacotherapy – psychotherapy – treatment resistant OCD)

3. INTRODUCTION Obsessive-compulsive disorder (OCD) is often a disabling condition consisting of intrusive thoughts that elicit a feeling of discomfort. To reduce the anxiety and distress associated with these thoughts, the patient may employ compulsions or rituals. These rituals are to compensate for the ego-dystonic feelings of the obsessional thoughts and can cause a significant decline in function. In (DSM)-5, obsessive-compulsive disorder sits under its own category of o bsessive-compulsive and related disorders  where the following subcategories were placed: Obsessive-compulsive disorder (OCD) * Body dysmorphic disorder (BDD) Hoarding disorder *Trichotillomania Excoriation (skin-picking) disorder Substance/medication-induced obsessive-compulsive and related disorder Obsessive-compulsive and related disorder as a result of another medical condition Other specified obsessive-compulsive and related disorder Unspecified obsessive-compulsive and related disorder

4. DSM5 :- OCRDs ARE Obsessive–compulsive disorder (OCD; previously classified as an anxiety disorder), body dysmorphic disorder (previously classified as a somatoform disorder) and trichotillomania (previously classified as an impulse control disorder), as well as hoarding disorder and excoriation (skin-picking) disorder (both of which are new to the classification system). * ICD-11 :- also includes Tourette syndrome (also classified as a neurodevelopmental disorder), hypochondriasis (also classified as an anxiety disorder) and olfactory reference syndrome (which is new to the classification system). * Some OCRDs include preoccupations and compulsive behaviors (such as body dysmorphic disorder), but others have predominantly motoric or behavioral symptoms (such as trichotillomania).

5. Obsessive-Compulsive Disorder Obsessive-compulsive disorder (OCD) is represented by a diverse group of symptoms that include intrusive thoughts, rituals, preoccupations, and compulsions. These recurrent obsessions or compulsions cause severe distress to the person. The obsessions or compulsions are time-consuming and interfere significantly with the person’s normal routine, occupational functioning, usual social activities, or relationships. OCD Patient may have obsession, a compulsion, or both. An obsession is a recurrent and intrusive thought, feeling, idea, or sensation. A compulsion is a conscious, standardized, recurrent behavior, such as counting, checking, or avoiding. In contrast to an obsession, which is a mental event, a compulsion is a behavior.

6. Obsessive Compulsive Disorder A patient with OCD realizes the irrationality of the obsession and experiences both the obsession and the compulsion as ego-dystonic (i.e., unwanted behavior). Although the compulsive act may be carried out in an attempt to reduce the anxiety associated with the obsession, it does not always succeed in doing so. The completion of the compulsive act may not a affect the anxiety, and it may even increase the anxiety. Anxiety is also increased when a person resists carrying out a compulsion.

7. What is happening with OCD patient?

8. EPIDEMIOLOGY The rates of OCD are fairly consistent, with a lifetime prevalence in the general population estimated at 2 to 3 percent. Some researchers have estimated that the disorder is found in as many as 10 percent of outpatients in psychiatric clinics. These figures make OCD the fourth most common psychiatric diagnosis after phobias, substance-related disorders, and major depressive disorder. Epidemiological studies in Europe, Asia, and Africa have confirmed these rates across cultural boundaries. Among adults, men and women are equally likely to be affected, but among adolescents, boys are more commonly affected than girls. The mean age of onset is about 20 years, although men have a slightly earlier age of onset (mean about 19 years) than women (mean about 22 years).

9. EPIDEMIOLOGY Overall, the symptoms of about two thirds of affected persons have an onset before age 25, and the symptoms of fewer than 15 percent have an onset after age 35. The onset of the disorder can occur in adolescence or childhood, in some cases as early as 2 years of age. Single persons are more frequently affected with OCD than are married persons, although this finding probably reflects the difficulty that persons with the disorder have maintaining a relationship. OCD occurs less often among blacks than among whites, although access to health care rather than differences in prevalence may explain the variation.

10. ETIOLOGY Biological Factors :- (1) Neurotransmitters *SEROTONERGIC SYSTEM. The many clinical drug trials that have been conducted support the hypothesis that dysregulation of serotonin is involved in the symptom formation of obsessions and compulsions in the disorder. Data show that serotonergic drugs are more effective in treating OCD than drugs that affect other neurotransmitter systems. Clinical studies have assayed cerebrospinal fluid (CSF) concentrations of serotonin metabolites (e.g., 5hydroxyindoleacetic acid [5-HIAA]) and affinities and numbers of platelet-binding sites of tritiated imipramine (Tofranil), which binds to serotonin reuptake sites, and have reported variable findings of these measures in patients with OCD. In one study, the CSF concentration of 5-HIAA decreased after treatment with clomipramine (Anafranil), focusing attention on the serotonergic system.

11. ETIOLOGY DOPAMINE (DA) Dopamine has a key role in stereotypic behavior *A decrease in striatal dopamine D2 receptors has been identified in patient with OCD. *limited data had suggested that dopamine synthesis increased in most regions of the cerebral cortex and cerebellum in OCD patients. *A hyperdopaminergic state is postulated to underpin OCD as evidenced by increased endogenous DA levels at baseline due to increased phasic firing at rest (and Tourette Syndrome which is commonly comorbid with OCD). *Dopamine neurons are known to represent Reward Processing Error (RPE) signals that can facilitate learning of reward predictions by the basal ganglia (striatum). *The dopaminergic neurons encode differences between rewards and expectations in the goal-directed system and differences between the chosen and habitual actions in the habit system. *This RPE processing plays an important role in action planning and decision-making.

12. ETIOLOGY * Evidence for Glutamatergic Involvement in OCD • Glutamine is excitatory neurotransmitter in cortico- striato - thalamo -cortical circuit • Increased caudate glutamate by MRS (Rosenberg et al, • Elevated CSF glutamate (Chakrabarty et al, Neuropsychopharm 2005 ) • Riluzole augmentation ( Coric et al, Biol Psych 2005). Riluzole is antiglutamatergic agent used in amyotrophic lateral sclerosis and augmentation in adult with refractory OCD. * NORADRENERGIC SYSTEM. Currently, less evidence exists for dysfunction in the noradrenergic system in OCD. Anecdotal reports show some improvement in OCD symptoms with use of oral clonidine (Catapres), a drug that lowers the amount of norepinephrine released from the presynaptic nerve terminals. *NEUROIMMUNOLOGY. Some interest exists in a positive link between streptococcal infection and OCD. Group A β- hemolytic streptococcal infection can cause rheumatic fever, and approximately 10 to 30 percent of the patients develop Sydenham’s chorea and show obsessive-compulsive symptoms.

13. PANDAS In rare cases ,sever OCD symptoms may suddenly appear in children ages 3-12 after an illness caused by streptococcal infection e.g. scarlet fever , sterpt. throat Streptococcal infections trigger an immune response, which in some individuals generates antibodies that cross-react with the basal ganglia. It is thought that the body’s natural response to infection, the production of certain antibodies, when directed to parts of the brain might be linked in some way to P ediatric A utoimmune N europsychiatric D isorders A ssociated with S treptococcal Infection ( PANDAS ). In addition to sudden or worsening OCD symptoms that appear along side a strept. Infection, the symptoms of PANDAS are (hyperactivity , fidgety, insomnia, bed wetting ,joint pain, mood swings, problem with motor skills, separation anxiety) What we do know is that if OCD results from a strep throat infection the symptoms will start quickly, probably within one or two weeks . PANDAS maybe not a cause for OCD, but triggers symptoms in children who are already predisposed to the disorder, perhaps through genetics or other causal explanations. Antibiotics may be used to treat underlying strpt . Infection alongside treatment for OCD.

14. ETIOLOGY (2) Brain Imaging Studies Neuroimaging in patients with OCD has produced converging data implicating altered function in the neurocircuitry between orbitofrontal cortex, caudate, and thalamus. Various functional brain-imaging studies—for example, positron emission tomography (PET)—have shown increased activity (e.g., metabolism and blood flow) in the frontal lobes, the basal ganglia (especially the caudate), and the cingulum of patients with OCD. The most supported neural and pathophysiological model of OCD focuses on overactivation of the cortico- striato - thalam - ocortica -circuits. According to this model, the orbitofrontal-subcortical pathway is hyperactive in OCD patients compared to healthy people, resulting in a change in the reinforcement contingencies of stimuli. Due to this change in reinforcement contingency , when OCD patients suffer from an obsession, they engage in some kind of behavior that reduces the anxiety or distress. Finally, they come to believe that this behavior is the solution to the obsession, and this learned behavior eventually becomes a compulsion .

15. BRAIN CIRCUITS INVOLVED IN (OCD) The cortico-striatal-thalamic-cortical loop (CSTC) is considered the critical brain circuit involved in the phenomenology of OCD. The CSTC circuits modulate several specific functions. Sensorimotor CSTC circuit. Supplementary motor area to putamen to the thalamus Stimulus-response-based habitual behavior (S-R)

16. BRAIN CIRCUITS INVOLVED IN (OCD) 2. Dorsal Cognitive CSTC circuit -Dorsolateral Prefrontal Cortex (DLPFC) & Dorsomedial Prefrontal Cortex (DMPFC) to caudate (dorsal) to thalamus. -Involved in working memory, planning and emotional regulation.

17. BRAIN CIRCUITS INVOLVED IN (OCD) 3. Frontoparietal network -Frontal cortex to the thalamus and parietal cortex -Coordination of cognitive control -Part of the alerting network

18. BRAIN CIRCUITS INVOLVED IN (OCD) 4. Ventral cognitive CSTC circuit Inferior frontal gyrus (IFG) and Ventrolateral Prefrontal cortex (VLPFC) to ventral caudate to thalamus. Involved in response inhibition.

19. BRAIN CIRCUITS INVOLVED IN (OCD) 5. Ventral motivational / reward CSTC circuit - Orbitofrontal cortex (OFC) to Nucleus Accumbens (NAc) to the thalamus - Involved in Stimulus outcome-based motivational behavior i.e. Stimulus-outcome (S-O)

20. BRAIN CIRCUITS INVOLVED IN (OCD) 6. Frontolimbic Network - VMPFC to amygdala to thalamus - Role in fear extinction

21. BRAIN CIRCUITS INVOLVED IN (OCD) 7. Frontal CSTC and Cerebellar Circuit -The cerebellum plays an important role in motor control and cognition. -OCD patients showed abnormal spontaneous cerebellar activity and weakened functional connectivity between the cerebellum and the CSTC circuit. -Decreased functional connectivity may result in an inability of the striatum to effectively inhibit the thalamus. -Excitation of the thalamus leads to hyperactivation of the direct excitatory CSTC.

22. B rian Circuits involved in OCD Obsessive–compulsive disorder (OCD) is mediated by parallel, partly segregated, cortico – striato – thalamo –cortical (CSTC) circuits that are involved in S ensorimotor , C ognitive, Affective and M otivational processes . dCaud , dorsal part of caudate nucleus; dlPFC , dorsolateral prefrontal cortex; dmPFC , dorsomedial prefrontal cortex; IFG, inferior frontal gyrus; NAc , nucleus accumbens; OFC, orbitofrontal cortex; pPut , posterior part of putamen; pre-SMA, pre-supplementary motor area; SMA, supplementary motor area; Tham , Thalamus; vCaud , ventral part of caudate nucleus; vlPFC , ventrolateral prefrontal cortex; vmPFC , ventromedial prefrontal cortex.

23. ETIOLOGY (3) Genetics. There is a genetic predisposition, as 45 to 65% of the variance of OCD is attributable to genetic factors. In mice and human experiments, mutated NMDA can cause an increase in OCD-like behavior. For example, mutations in the NMDA subunit “NR2” have been linked to fears of contamination and compulsive cleaning OCD does appear to be heritable, confirmed by both twin and family studies. Research has shown the heritability to be as high as 45% to 65% in children and 27% to 45% in adults. OCD has links with other neurological disorders, particularly those that affect the cortico- striato - thalamo-cortico circuits, such as Parkinson disease, Sydenham chorea, traumatic brain injury (TBI), Tourette syndrome, Huntington disease, and epilepsy. Studies of concordance for the disorder in twins have consistently found a significantly higher concordance rate for monozygotic twins than for dizygotic twins. Some studies also demonstrate increased rates of a variety of conditions among relatives of OCD probands, including generalized anxiety disorder, tic disorders, body dysmorphic disorder, hypochondriasis, eating disorders, and habits such as nail-biting.

24. ETIOLOGY Genetic Specific genes associated with OCD:- *SERT (Serotonergic) *COMT (Dopaminergic) *SLC1A1and GRIN2B (Glutamatergic) *GRID2 and DLGAP1 (Glutamatergic) *Insulin signaling genes A significant association between autosomal OCD genes centered around CNS insulin-regulated synaptic function and ‘symmetry/counting/ordering’. Peripheral insulin signaling link between Type 2 diabetes (T2D) and aggressive taboo thoughts and T2D and contamination/cleaning. Genetic factors contribute to specific OCS dimensions, including contamination/cleaning and checking/ordering. Additive genetic effects account for ~40% of the variance, and the non-shared environment accounts for ~51% of the variance. Early-onset OCD with tics may have a higher heritability. 50% of these deletions were located in a single locus 16p13.11.

25. ETIOLOGY (4) Other Biological Data. Electrophysiological studies, sleep electroencephalogram (EEG) studies, and neuroendocrine studies have contributed data that indicate some commonalities between depressive disorders and OCD. Sleep EEG studies have found abnormalities similar to those in depressive disorders, such as decreased rapid eye movement latency. Neuroendocrine studies have also produced some analogies to depressive disorders, such as non suppression on the dexamethasone-suppression test in about one-third of patients and decreased growth hormone secretion with clonidine infusions. As mentioned, studies have suggested a possible link between a subset of OCD cases and certain types of motor tic syndromes (i.e., Tourette’s disorder and chronic motor tics). Most family studies of probands with OCD have found increased rates of Tourette’s disorder and chronic motor tics only among the relatives of probands with OCD who also have some form of tic disorder. Evidence also suggests cotransmission of Tourette’s disorder, OCD, and chronic motor tics within families.

26. ETIOLOGY *Summery of biological factors By evaluating individuals who develop OCD , we were able to localize OCD symptoms to certain areas of the brain. Through fMRIs, DTI, and SPECT imaging, OCD has been observed to be linked to the ( CSTC ) cortico- striato - thalamo -cortical circuits, particularly the orbitofrontal cortex, the caudate, anterior cingulate cortex, and thalamus. There is likely dopaminergic and glutamatergic overactivity in frontostriatal pathways and diminished serotonergic and GABAergic neurotransmission in frontolimbic systems.

27. ETIOLOGY Psychological factors Behavioral theory of OCD (learning Theory) * Some research suggests that people with OCD have developed negative associations with certain kinds of stimuli over time. *These negative associations may have conditioned them to have a fear response even when there is no real threat. These researchers elegantly specified the behavioral theory of OCD, that “obsessional thoughts have through conditioning, become associated with anxiety that has failed to extinguish”. * Certain learned behaviors in response to anxiety may play a role in developing OCD symptoms. *For example, someone with OCD may adopt avoidance behaviors, such as going out of their way to avoid germs, to deal with emotional distress. * ERP treatment for OCD begins with understanding the formation of the obsession and compulsion by applying learning theory (classical conditioning and operant conditioning).

28. Behavioral theory Classical conditiong theory :- suggests that, in OCD patients, a neutral stimulus can be overgeneralized and become a CS that evokes obsession. For example, a patient who has an obsession with contamination fears contamination by stimuli that healthy people would not think are dirty. Understanding classical conditioning while performing the therapy is helpful when planning ERP therapy. ERP can be more effective if the therapist understands the factors (who, when, where, what, and how) that cause the obsession and can therefore clarify all aspects of the obsessive pattern, i.e., the CS, unconditioned stimulus (US), unconditioned response (UR), and conditioned response (CR) Psychotherapy aims to help people with OCD get out of this negative cycle of thinking and behavior. Behavioral therapy can help people with OCD develop healthier coping skills.

29. Behavioral theory ( Compulsion and operant conditioning ) The formation of a compulsion can be explained by the theory of operant conditioning. The Skinner box became an important tool for studying learned behavior and contributed a great deal to our understanding of the effects of reinforcement and punishment. OCD patients judge that a ritual behavior relieves the anxiety or distress caused by an obsession. This belief leads them to engage in the behavior, which is then reinforced, increasing the likelihood that the compulsive behavior will occur again when the obsession recurs. For example, patients repeatedly wash their hands to reduce anxiety whenever they think their hands are dirty or contaminated. Operant conditioning is also applied to understand the mechanism of habituation when carrying out ERP treatment. ERP approaches are habituation-based models that emphasize reduction in fear through the exposure and response-prevention process as essential for reducing symptoms.

30. Cognitive Theory of OCD Obsessional thoughts :- - if obsessions occur frequently in normal populations. Why don’t most people suffer from OCD ? - It does not the thought itself is disturbing , but rather the interpretation of the thought. Example: having an unacceptable sexual thought leads to beliefs that the person is depraved, perverted, abnormal, evil, etc. ….. Which leads to affective states such as anxiety and depression. The issue of responsibility is believed to be a core belief or cognitive distortion of people with OCD.

31. Cognitive Theory of OCD It believes that individuals with OCD have faulty beliefs, and that it is their misinterpretation of intrusive thoughts that leads to OCD. According to the cognitive model of OCD, everyone experiences intrusive thoughts from time-to-time. However, people with OCD often have an inflated sense of responsibility and misinterpret these thoughts as being very important and significant which could lead to catastrophic consequences. The repeated misinterpretation of intrusive thoughts leads to the development of the obsessions and because the thoughts are so distressing, the individual engages in compulsive behavior to try to resist, block, or neutralize the obsessive thoughts. The cognitive-behavioural theory builds on behavioural theory as it begins with an identical proposition that obsessional thinking has its origins in normal intrusive cognitions. However, in the cognitive theory the difference between normal intrusive cognitions and obsessional intrusive cognitions lies not in the occurrence or even the (un)controllability of the intrusions themselves, but rather in the interpretation made by people with OCD about the occurrence and/or content of the intrusions.

32. Psychodynamic Theory

33. Psychodynamic theory

34. PSYCHOANALTIC THEORY SIGMUND FREUD. In classic psychoanalytic theory, OCD was termed obsessive-compulsive neurosis and was considered a regression from the oedipal phase to the anal psychosexual phase of development.

35. PSYCHOANALYTIC THEORY

36. When patients with OCD feel threatened by anxiety about retaliation for unconscious impulses or by the loss of a significant object’s love, they retreat from the oedipal position and regress to an intensely ambivalent emotional stage associated with the anal phase. Ambivalence . Ambivalence is an important feature of normal children during the analsadistic developmental phase; children feel both love and murderous hate toward the same object, sometimes simultaneously. This conflict of opposing emotions is evident in a patient’s doing and undoing patterns of behavior and in paralyzing doubt in the face of choices. Magical Thinking. In magical thinking, regression uncovers early modes of thought rather than impulses; that is, ego functions as well as id functions are affected by regression. Omnipotence of thought is magical thinking :- Persons believe that merely by thinking about an event in the external world they can cause the event to occur without intermediate physical actions. This feeling causes them to fear having an aggressive thought

37. SUMMRY OF PSYCHOLOGICAL THEORIES OF OCD

38. ETIOLOGY (ENVIROMENTAL FACTORS) *Stress and parenting styles are environmental factors. T hat have been blamed for causing OCD, but no evidence is yet to show that. Stress does not actually cause OCD, but major stresses or traumatic life events may precipitate the onset of OCD. However, these are not thought to cause OCD, but rather trigger it in someone already predisposed to the disorder. If left untreated, everyday anxiety and stress in a person’s life will worsen symptoms in OCD. Problems at school or work, university exam pressures and normal everyday problems that relationships can bring are all contributory factors to increasing the frequency and severity of a person’s OCD. Research suggests that OCD may be precipitated by a number of environmental stressors, especially those involving pregnancy, childbirth, or parental care of children.

39. Diagnosis and Clinical F eature

40. Diagnosis and Clinical F eature

41. Diagnosis and Clinical F eature As part of the diagnostic criteria for OCD, the (DSM-5) allows clinicians to indicate whether the patient’s OCD is characterized by good or fair insight, poor insight, or absent insight. Patients with good insight recognize that their OCD beliefs are definitely not true or may not be true. Patients with poor insight believe their OCD beliefs are probably true, and patients with absent insight are convinced that their beliefs are true. Most patients with OCD have both obsessions and compulsions—up to 75 percent in some surveys. Some researchers and clinicians believe that the number may be much closer to 100 percent if patients are carefully assessed for the presence of mental compulsions in addition to behavioral compulsions. For example, an obsession about hurting a child may be followed by a mental compulsion to repeat a specific prayer a specific number of times. Other clinicians believe that some patients do have only obsessive thoughts without compulsions. Such patients are likely to have repetitious thoughts of a sexual or aggressive act that is reprehensible to them.

42. Symptom Patterns of obsessions and compulsions in adults and in children Major Presenting Symptom ( ADULT) % Obsession s (N = 2 0 0) *Contamination *Pathologic doubt *Somatic *Need for symmetry *Aggressive *Sexual *Other *Multiple obsessions Compulsions (N = 2 0 0) *Checking *Washing *Counting *Need to ask or confess *Symmetry and precision *Hoarding *Multiple comparisons 4 5 4 2 3 6 3 1 2 8 2 6 1 3 6 0    6 3 5 0 3 6 3 1 2 8 1 8 4 8 Major Presenting Symptom No. (%) Children Obsession * Concern or disgust with bodily wastes or secretions (urine, stool, saliva), dirt, germs, environmental toxins. *Fear something terrible may happen (fire, death or illness of loved one, self, or others). *Concern or need for symmetry, order, or exactness. *Scrupulosity (excessive praying or religious concerns out of keeping with patient’s background). *Lucky and unlucky numbers *Forbidden or perverse sexual thoughts, images, or impulses. *Intrusive nonsense sounds, words.   30 (43)      18 (24)   12 (17)   9 (13)  6 (8) 3 (4)   1 (1)

43. Symptom Patterns of obsessions and compulsions in adults and in children Major Presenting Symptom ( ADULT) % Major Presenting Symptom No. (%) Children Compulsions (N = 2 0 0) - Checking -Washing -Counting -Need to ask or confess -Symmetry and precision -Hoarding -Multiple comparisons Course of illness (N = 1 0 0) -A Type Continuous -Deteriorative -Episodic -Not present 6 3 5 0 3 6 3 1 2 8 1 8 4 8 8 5 10 2 71 Compulsion -Excessive or ritualized handwashing, showering, bathing, toothbrushing, or grooming. -Repeating rituals (e.g., going in and out of door, up and down from chair). -Checking doors, locks, stove, appliances, car brakes. -Cleaning and other rituals to remove contact with contaminants. -Touching. -Ordering and arranging. 60 (85)   36 (51)  32 (46)   16 (23) 14 (20) 12 (17)

44. The symptoms of patient can overlap and change with time, but OCD has four major symptom patterns. Contamination . The most common pattern is an obsession of contamination, followed by washing or accompanied by compulsive avoidance of the presumably contaminated object. The feared object is often hard to avoid (e.g., feces, urine, dust, or germs). Patients may literally rub the skin off their hands by excessive hand washing or may be unable to leave their homes because of fear of germs. Although anxiety is the most common emotional response to the feared object, obsessive shame and disgust are also common. Patients with contamination obsessions usually believe that the contamination is spread from object to object or person to person by the slightest contact. Pathological Doubt. The second most common pattern is an obsession of doubt, followed by a compulsion of checking. The obsession often implies some danger of violence (e.g., forgetting to turn off the stove or not locking a door). The checking may involve multiple trips back into the house to check the stove, for example. These patients have an obsessional self-doubt and always feel guilty about having forgotten or committed something.

45. Intrusive Thoughts. In the third most common pattern, there are intrusive obsessional thoughts without a compulsion. Such obsessions are usually repetitious thoughts of a sexual or aggressive act that is reprehensible to the patient. Patients obsessed with thoughts of aggressive or sexual acts may report themselves to police or confess to a priest. Suicidal ideation may also be obsessive; but a careful suicidal assessment of actual risk must always be done. Symmetry . The fourth most common pattern is the need for symmetry or precision, which can lead to a compulsion of slowness. Patients can literally take hours to eat a meal or shave their faces. Other Symptom Patterns. Religious obsessions and compulsive hoarding are common in patients with OCD. Compulsive hair pulling and nail biting are behavioral patterns related to OCD. Masturbation may also be compulsive.

46. TYPES OF OCD

47. Mental Status Examination On mental status examinations, patients with OCD may show symptoms of depressive disorders. Such symptoms are present in about 50 percent of all patients. Some patients with OCD have character traits suggesting obsessive-compulsive personality disorder (e.g., excessive need for preciseness and neatness), but most do not. Patients with OCD, especially men, have a higher-than-average celibacy rate. Married patients have a greater than usual amount of marital discord.

48. Psychometric Assessment * It is essential to screen for the correct symptoms of obsessive-compulsive disorder. * A common tool and the most widely accepted tool to screen for OCD is the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). *The Y-BOCS rates on a scale from 0 to 40 (40 being the most severe of symptomatology). *It requires the patient to rank, based on severity: • The time occupied by obsessive thoughts and compulsions • The interference of obsessive thoughts • The distress of obsessive thoughts • Resistance against obsessions • Degree of control over obsessive thoughts • The time occupied by compulsive behavior • The interference of compulsive behavior • The distress associated with compulsive behavior • Resistance against compulsive behavior • Degree of control over compulsive behaviors

49. Comorbidity Many people with OCD have comorbid neurological and psychiatric disorders (Comorbid means they can occur alongside OCD). The lifetime prevalence for major depressive disorder in persons with OCD is about 67 percent and for social phobia about 25 percent. The incidence of Tourette’s disorder in patients with OCD is 5 to 7 percent, and 20 to 30 percent of patients with OCD have a history of tics. Other common comorbid psychiatric diagnoses in patients with OCD include alcohol use disorders, generalized anxiety disorder, specific phobia, panic disorder, eating disorders, and personality disorders. OCD exhibits a superficial resemblance to obsessive-compulsive personality disorder, which is associated with an obsessive concern for details, perfectionism, and other similar personality traits.

50. Comorbidity The prevalence of comorbid mental disorders in patients with obsessive–compulsive disorder (OCD)

51. DIFFERENTIAL DIAGNOSIS Medical Conditions A number of primary medical disorders can produce syndromes bearing a striking resemblance to OCD. The current conceptualization of OCD as a disorder of the basal ganglia derives from the phenomenological similarity between idiopathic OCD and OCD like disorders that are associated with basal ganglia diseases, such as Sydenham’s chorea and Huntington’s disease. Neurological signs of such basal ganglia pathology must be assessed when considering the diagnosis of OCD in a patient presenting for psychiatric treatment. It should also be noted that OCD frequently develops before age 30 years, and new-onset OCD in an older individual should raise questions about potential neurological contributions to the disorder. Tourette’s Disorder In its classic form, Tourette’s disorder is a nervous system disease associated with a pattern of repetitive & recurrent vocal and motor tics (involuntary twitches movements and sounds ). OCD is closely related to Tourette’s disorder, as the two conditions frequently co-occur, both in individuals over time and within families. About 90 percent of persons with Tourette’s disorder have compulsive symptoms, and as many as two thirds meet the diagnostic criteria for OCD.

52. DIFFERENTIAL DIAGNOSIS The premonitory urges that precede tics often strikingly resemble obsessions, however, and many of the more complicated motor tics are very similar to compulsions. Obsessive compulsive personality disorder The conditions are easily distinguished in that only OCD is associated with a true syndrome of obsessions and compulsions. OCPD OCD It is a form of personality disorders It is a form of Obsessive compulsive related disorders

53. DIFFERENTIAL DIAGNOSIS ADHD :- 12%o of adult with OCD have ADHD. Among children comorbid ADHD with OCD are more common, over 25%of children with OCD have ADHD as well. Other Psychiatric Conditions Obsessive-compulsive behavior is found in a host of other psychiatric disorders, and the clinician must also rule out these conditions when diagnosing OCD. Psychotic symptoms often lead to obsessive thoughts and compulsive behaviors that can be difficult to distinguish from OCD with poor insight, in which obsessions border on psychosis. The keys to distinguishing OCD from psychosis are patients with OCD can almost always acknowledge the unreasonable nature of their symptoms, and psychotic illnesses are typically associated with a host of other features that are not characteristic of OCD. Similarly, OCD can be difficult to differentiate from depression because the two disorders often occur comorbidly, and major depression is often associated with obsessive thoughts that, at times, border on true obsessions such as those that characterize OCD. The two conditions are best distinguished by their courses. Obsessive symptoms associated with depression are only found in the presence of a depressive episode, whereas true OCD persists despite remission of depression. 76% of people with OCD have anxiety disorders as GAD

54. COURSE AND PROGNOSIS More than half of patients with OCD have a sudden onset of symptoms. The onset of symptoms for about 50 to 70 percent of patients occurs after a stressful event, such as a pregnancy, a sexual problem, or the death of a relative. Because many persons manage to keep their symptoms secret, they often delay 5 to 10 years before coming to psychiatric attention, although the delay is probably shortening with increased awareness of the disorder. The course is usually long but variable; some patients experience a fluctuating course, and others experience a constant one. About 20 to 30 percent of patients have significant improvement in their symptoms, and 40 to 50 percent have moderate improvement. The remaining 20 to 40 percent of patients either remain ill or their symptoms worsen. Obsessive-compulsive disorder (OCD) is named one of the top ten disabling disorders by the WHO.

55. COURSE AND PROGNOSIS About one-third of patients with OCD have major depressive disorder, and suicide is a risk for all patients with OCD. A poor prognosis is indicated by due to (rather than resisting) compulsions, childhood onset, bizarre compulsions, the need for hospitalization, a coexisting major depressive disorder, delusional beliefs, the presence of overvalued ideas (i.e., some acceptance of obsessions and compulsions), and the presence of a personality disorder (especially schizotypal personality disorder). A good prognosis is indicated by good social and occupational adjustment, the presence of a precipitating event, and an episodic nature of the symptoms. The obsessional content does not seem to be related to the prognosis. Obsessive-compulsive disorder (OCD) typically is a lifelong illness, though some experience a waxing and waning course. Even with CBT and/or SSRIs, seldom do the symptoms ever resolve. Roughly 30% of patients refuse treatment, abort treatment, or fail to respond to treatment. Of those who have successful treatment, about 50% have residual symptoms. Co-occurring hoarding has a worse prognosis.

56. COURSE AND PROGNOSIS As reported by the adult psychiatric morbidity survey, an association between OCD and suicide has been established and has links to comorbid anxiety, depression, and past suicide attempts. A cross-sectional study from January 2019 found that OCD and suicide are related regardless of symptoms of depression or mood instability. If OCD does not get treated, the course is typically chronic, and it may be an episodic course, with a minority having a deteriorating course. Onset in childhood or adolescence can lead to chronic disease. However, 40% of individuals with the onset of OCD in childhood or adolescence experience remission by early adulthood. Other disorders often complicate the course of OCD. In (OCD), the patient's insight is not lacking. Only 2% to 4% lack insight into their OCD. However, most people do not seek treatment until well into their disorder. This fact may lead to a decrease in social interactions and a poor quality of life.

57. TREATMENT Treatment of OCD consists of pharmacological , psychological and neuromodulation techniques . Historically the tricyclic antidepressant (TCA) clomipramine was used as the first line for OCD due to its strong predilection for serotonin. Clomipramine was approved for OCD in the late 80s but is no longer the first line to treat OCD, given its complicated side effect profile and the potential to elicit arrhythmias, seizures, and anticholinergic side effects to name a few. However, given the side effect profile, SSRIs have gained favor. OCD is most commonly treated with SSRIs, and at much higher doses than used to treat anxiety or depression. FDA-approved SSRIs include fluoxetine, fluvoxamine, paroxetine, and sertraline Two primary neurotransmitters thought to contribute to OCD are serotonin and glutamate. The serotonin hypothesis came after reducing OCD symptoms with the use of serotonergic antidepressants.

58. TREATMENT Glutamate hypotheses has been gaining support as more data comes to light. The use of d- cycloserine (DCS), a partial NMDA receptor agonist (a glutamate receptor), has gathered attention as research has shown DCS to enhance extinction learning in animal studies. Other medications currently investigated include memantine, lamotrigine, N-acetyl cysteine, ketamine, topiramate, glycine, and riluzole, though more studies are necessary to prove their efficacy. Antipsychotics have been entertained as adjunct therapy. Aripiprazole, haloperidol and risperidone were significantly superior to placebo. The following are appropriate drugs and doses typically used to treat OCD: * fluoxetine 80 mg, escitalopram 40 mg, fluvoxamine 300 mg, and paroxetine 100 mg. *Citalopram is no longer a recommended agent, given the risk of QTc prolongation in higher doses. * Those treated with an SSRI for OCD will need a longer trial of 8 to 12 weeks on the medication as they typically take longer to respond than those receiving treatment for depression for a reason still unknown.

59. TREATMENT Treatment with SSRIs can be augmented with the use of the NMDA receptor antagonist memantine. In a double-blinded controlled study in Iran, memantine was beneficial; after eight weeks of treatment, there was a 100% response with 89% remission. Other medications that have been tried for OCD modulation via the NMDA receptors include topiramate, lamotrigine, ketamine, and riluzole, but so far, data has been inconclusive. Other medications being explored as augmentation therapy include ondansetron, tramadol, and amphetamines; however, no conclusive evidence can be drawn at this time. There have been instances of refractory cases having treatment with ablative lesion neurosurgery; however, there are no controlled trials. Transcranial magnetic stimulation (TMS) has not proven successful in treating the disorder Deep brain stimulation has also been considered for severe cases of refractory OCD. D eep brain stimulation is still a novel treatment, and due to the high costs and invasive nature of the procedure is not yet in routine use. Over the past 20 years, only 200 to 300 patients with OCD have received treatment with DBS. In an Amsterdam study published in October 2019, they found that DBS aimed at the ventral anterior limb of the internal capsule makes those with OCD more open to environmental change and can engage in more activities than their compulsions.

60. PSYCHOTHERAPY ( OCD ) - Although a systemic review and meta- analysis showed that CBT has been to be more effective than SSRIs in clinical practice both SSRIs and CBT are often used together. - Both individual and group CBT are as effective as each other. - CBT comprises two components *Cognitive reappraisal *Behavioral intervention :- exposure – response prevention (ERP)is psychological treatment of choice for OCD (ERP – CBT) ERP involves (a) exposed the patient to stimuli that provoke the obsessional response, and (b) helped the patient to prevent avoidance and escape (compulsive) responses. How :- The patient is learnt to face situations that would provoke obsessions and associated anxiety and distress. The patient is learnt to resist the associated compulsions or avoidance behaviors. When the compulsions were delayed or prevented, people with OCD experienced a spontaneous decay in anxiety and the urges to perform compulsions. Continued practice led to the extinction of anxiety.

61. PSYCHOTHERAPY   The goal is to restructure the mind and alter the habituation created by participating in the compulsion. Integration of ERP with cognitive components, e.g discussion of feared consequences and dysfunctional beliefs, can make ERP less aversive and enhance its effectiveness particularly for patients with poor insight and for those who are less tolerant to exposure. Recommended 13 to 20 weekly sessions or 3 weeks of daily sessions. If necessary, additional sessions can then be offered to the patient 3 to 6 months after the first session. Patient adherence to between-session homework, e.g doing ERP exercises in the home environment is the most robust predictor of good short and long-term response. The psychological mechanisms underpinning this technique are habituation and extinction . * Habituation is the decline in response after repeated exposure to a stimulus. * Extinction refers to the cessation or reduction of behavior when a reinforcer is taken away or ceases .

62. PHARMACOTHERAPY (OCD ) SSRIs are considered the first line in the treatment of OCD. Approximately 50 % of patients respond to the first line treatment. Mechanism of SSRIs in OCD Reduction of rumination and/or anxiety symptoms, positive shift in the appraisal of emotions and improved fear extinction through action on the amygdala improving OCD symptoms and increasing the possibility of response to exposure treatment aimed at extinguishing maladaptive compulsive habits and irrational fears. A recent meta-analysis showed that a significant benefit from SSRIs treatment after 2 weeks from the start of treatment suggesting that the greatest incremental treatment gains in OCD are seen early on in SSRI treatment Equivalent doses of other SSRIs and clomipramine at Fluoxetine dose of 20 mg : Fluvoxamine: 100 mg Sertraline: 50 mg Paroxetine: 20 mg Citalopram: 20mg Escitalopram:10 mg Clomipramine: 100mg

63. PHARMACOTHERAPY IN OCD High – dose SSRIs Maximum dose SSRIs High-dose SSRIs have been shown to be more effective than lower doses. SSRIs should be prescribed for at least 12 weeks to determine responsiveness Fluoxetine: 20-80 mg/day Fluvoxamine: 100-300 mg/day Sertraline: 50-200 mg/day Paroxetine: 20-60 mg/day Citalopram: 20-60 mg Escitalopram: 10-40 mg/day Used in patients who are * rapid metabolizers *No or mild side effects *Inadequate response after 8 weeks or more with usual high dose Fluoxetine: 120mg/day Fluvoxamine: 400 mg/day Sertraline: 400 mg/day Paroxetine: 100mg Citalopram: 120mg Escitalopram: 60mg/day

64. PHARMACOTHERAPY ( OCD) Sertraline : A rapid sertraline titration of up to 200 mg/day correlated with fast response rates. Higher doses of 250mg -400 mg have shown efficacy in refractory OCD. Escitalopram : The most 5-HT-selective among SSRIs with little or no affinity for other neurotransmitter transporter or receptors. 20 mg/day escitalopram has also been associated with better OCD symptom remission compared to 40 mg/day paroxetine or placebo at week 12 Higher doses of > 20 mg may be associated with QTc prolongation. Weak or minimal interactions with the cytochrome P450 system Citalopram : Risk of QTc interval prolongation with doses above 40 mg /day Fluvoxamine : CYP1A2 inhibitor which may interact with other medications. Long-term treatment (40 weeks with a dose of 100-300 mg/day) was associated with improvements in psychosocial skills and obsessive symptoms.

65. PHARMACOTHERAPY ( OCD ) Clomipramine: Clomipramine is used as a second or third-line agent in OCD treatment. Some evidence supports the add-on of clomipramine to an SSRI before trying an antipsychotic add-on treatment. Clomipramine is a tricyclic antidepressant, which acts as a serotonin and noradrenaline reuptake inhibitor with a stronger affinity for the serotonin transporter (SERT) than other TCAs and SSRIs T he resulting action increases serotonergic and noradrenergic transmission. Clomipramine is metabolized to its active metabolite desmethylclomipramine by CYP450 1A2. Desmethylclomipramine has more noradrenergic activity than serotonergic. Treatment response is significantly is corelated with higher plasma clomipramine and a trend toward lower desmethylclomipramine. Clomipramine is started at 25 mg/day and increased to a target dose of 250 mg/day. Clomipramine tolerability is affected by its significant anticholinergic side effects (dry mouth, blurred vision, fatigue, tremor and hyperhidrosis). Amongst severe side effects, arrhythmogenic potential and risk of seizures increase at doses at or above the upper limit of the recommended dosing range (250 mg). ECG monitoring is recommended

66. PHARMACOTHERAPY ( OCD ) Combined levels of clomipramine and desmethylclomipramine should be kept below 500 ng/ml to minimize the risk of seizures and arrhythmias. Clomipramine (≤75 mg/day) addition to fluoxetine ( ≤40 mg/day) was a safe and effective treatment for fluoxetine non responders and for those who could not tolerate a high dose of fluoxetine. This combination was also superior to augmenting fluoxetine with quetiapine. Citalopram (maximum dose of 60 mg/day) augmentation of Clomipramine in treatment-refractory OCD showed that approximately 50% of the patients improved significantly after 1 month of this regimen and after 1 year of treatment. Other antidepressants: SNRIs Venlafaxine (225 to 350 mg/day) has shown similar efficacy to clomipramine in the short-term treatment of OCD with better tolerability. Most studies have shown efficacy in both naïve and treatment resistant OCD patients at dosages between 150 mg/day and 375mg/day with 30-60%response rates.

67. PHARMACOTHERAPY ( OCD) Venlafaxine 300 mg/day showed similar response rates to Paroxetine (60 mg/day) in non-refractory OCD although paroxetine may be more effective than venlafaxine in refractory patients. Duloxetine and milnacipran have shown some evidence. Approximately 25% of all OCD patients will be classified as treatment resistant this is defined as failing 2 different SSRIs course. . Furthermore, 40-60% of all patients may be considered as responding positively to treatment but will have ongoing residual symptoms. Agomelatine Agomelatine 5-HT2C antagonism mediates anxiolytic effects which indirectly improves OCD symptoms Melatonin (MT1 and MT2 receptors agonist activity) could contribute to circadian rhythm restoration in OCD patients.

68. TREATMENT OF RESISTANT AND REFERACTORY OCD Factors associated with poor treatment response: Clinical characteristics -Greater severity -Sexual, religious and hoarding symptoms -Poor insight -Higher number of comorbidities -Comorbid major depression, agoraphobia or social anxiety disorder -Lower willingness to fully experience unpleasant thoughts -Greater resistance to change -Lower adherence to treatment Factors associated with poor treatment response: Sociodemographic characteristics - Male sex - Single relationship status - Lower socioeconomic status - Lower educational level Other characteristics - Family history of OCD - Poor therapeutic alliance - Greater family accommodation - Absence of early response to selective serotonin reuptake inhibitor treatment.

69. TREATMENT OF RESISTANT AND REFERACTORY OCD Approximately 25% of all OCD patients will be classified as treatment resistant OCD :this is defined as failing of 2 different SSRIs course of treatment Furthermore, 40-60% of all patients may be considered as responding positively to treatment but will have ongoing residual symptoms. A patient meets the criteria for OCD resistant when he or she has a reduction inferior to 25% at the YBOCS despite a trial of at least 12 weeks at the highest tolerated dose of SSRIs or clomipramine, in combination with at least 30 h of CBT. Refractory OCD is defined as a non-response after 3–6 months of at least three antidepressants (including clomipramine), and at least two add-on trial with atypical antipsychotics Strategies in Treatment Refractory OCD: High-dose treatment with serotonergic drugs Greater improvement with higher vs lower doses of SSRI e.g 250 to 400 mg/day vs 200 mg/day of sertraline and with escitalopram after an increase of dose from 20 up to 50 mg/d. Approximately 25% of patients with refractory OCD to SSRIs may benefit from up to128 weeks treatment after initiation.

70. TREATMENT OF RESISTANT AND REFERACTORY OCD Antipsychotics Augmentation with antipsychotics is effective in 30% of treatment resistant patients. Augmentation agents to SSRIs / CBT in refractory OCD. Haloperidol, risperidone and aripiprazole are effective. In one study, olanzapine, paliperidone, and quetiapine could not differentiate from placebo as measured by mean Y-BOCS total improvement. Haloperidol is also an effective augmentation agent in OCD with comorbid tics The World Federation of Societies of Biological Psychiatry (WFSBP) recommended a co-administration of SSRI with haloperidol, quetiapine, olanzapine or risperidone for treatment-resistant OCD. *Aripiprazole 5-10 mg/day *Risperidone 1-3 mg/day *Haloperidol 2.5-10 mg/day * Olanzapine 5-10 mg/day The most supported evidence was for lamotrigine, memantine, and aripiprazole. If an antipsychotic must be used and aripiprazole is not tolerated, risperidone may be considered as an alternative.

71. TREATMENT OF RESISTANT AND REFERACTORY OCD Memantine 10-20 mg/day as add on. a NMDA receptor antagonist which regulates the effects of pathologically elevated glutamate levels in OCD Memantine has shown benefits in trichotillomania and skin picking disorder which can coexist with OCD but are distinct conditions. Lamotrigine 100 mg/day is an antiepileptic drug used in the maintenance treatment of bipolar disorder. In view of its inhibitory action on AMPA glutamatergic receptors, it may have a role as an adjunctive therapy in OCD Topiramate up to 400 mg/day- topiramate at daily dose ranges up to 400 mg improved refractory OCD. Topiramate, another AMPA antagonist, showed controversial results as both improvements and worsening of symptoms were observed. D- cycloserine :- D- cycloserine : Partial agonism at the site of glycine recognition of the NMDA receptor, which is linked in the amygdala to learning and memory, could be the basis of the mechanism of action of D- cycloserine . Ketamine :- Ketamine is a NMDA receptor antagonist as well as a nonselective agent targeting the opioid, cholinergic and monoamine systems, all of which may contribute to its efficacy in OCD

72. TREATMENT OF RESISTANT AND REFERACTORY OCD Riluzole:- is antiglutamatergic agent used in ALS and augmentation in adult with refractory OCD. 5 HT-3 Antagonists: 5-HT3 blockade produces a weak inhibitory effect on dopaminergic neurotransmission Ondansetron (1-8 mg/day) is a potential augmenting agent in patients for whom SGAs are problematic Opiods :- Add-on buprenorphine (400-600 μ g/day sublingual) to SSRIs; 200 mg/day fluvoxamine or 200 mg/day sertraline or 150 mg/day clomipramine resulted in a significant improvement in the proportion of refractory patients, particularly in people who partially responded to SSRIs 200-400 μg /day sublingual add-on buprenorphine to SSRIs or clomipramine showed symptom reduction in as early as 3 weeks suggesting the addition of buprenorphine may accelerate treatment response Dopaminergic agonists :-Acute significant antiobsessional effects for a single dose of dextroamphetamine were reported in patients with severe OCD. Augmentation with serotonergic antidepressants in refractory OCD showed improvement in OCD.

73. NEUROMODULATION THERAPIES Neurosurgery Ablative neurosurgery involves producing lesions in specific regions of the CSTC circuit. Neurosurgery is indicated in only severe cases of OCD. Approximately 60 per cent of patients improve 6-24 months post-surgery. Key techniques for surgery are: -anterior cingulotomy -capsulotomy - subcaudate tractotomy -limbic leucotomy (combination of anterior cingulotomy & capsulotomy) Deep Brain Stimulation (DBS) Non ablative surgical techniques involving indwelling electrodes in various basal ganglia nuclei are under investigation to treat both OCD and Tourette’s disorder. DBS is performed using MRI-guided stereotactic techniques in which electrodes are implanted in the brain.

74. DBS is reversible and can be adjusted postoperatively in the outpatient clinic. In DBS, once the electrodes have been implanted, they generate continuous electrical stimulation through a pulse generator The impulse generator is also referred to as a ‘brain pacemaker’ and has a battery life of up to 15 years for those with externally rechargeable batteries. Most studies of DBS in OCD target striatal areas, including the anterior limb of the internal capsule, the ventral capsule and ventral striatum, the nucleus accumbens or the ventral caudate nucleus, the subthalamic nucleus, and the inferior thalamic peduncle. Approximately 30–60% of patients with severe refractory OCD respond to these different treatments. Proposed mechanisms may include normalization of excessive baseline frontostriatal activity and normalization of low baseline Complications of DBS include infection, bleeding, or the development of seizures, which are almost always controlled by treatment with phenytoin (Dilantin)

75. Repetitive Transcranial Magnetic Stimulation ( rTMS ): The regions associated with OCD are not usually accessible by rTMS . However, there is some evidence of efficacy. rTMS targets include the supplementary motor cortex and the DLPFC. The quality of evidence is currently low Transcranial Direct Current Stimulation ( tDCS ): Targets are the supplementary motor cortex and the dorsolateral prefrontal cortex. Some promises but no RCTs. Treatment for PANDAS / PANS Psychotherapy and psychopharmacological treatments are first line For treatment-resistant patients anti-microbial agents (antibiotics, anti- virals and anti-parasitic agents) For moderate to severe symptoms: steroids or intravenous immunoglobulins (IVIGs). For severe or chronic presentations: prolonged steroid trials or repeated high-dose steroids may be indicated. Children with PANDAS who have a severe form and/or recurrent courses of streptococcus-associated exacerbations or an initial manifestation: Antibiotic prophylaxis.

76. Thank you