Concept of Spectrum

• In Psychiatry – Qualitatively different but related to one pathogenic link.

Psychiatric usage:
• • Spectrum/ dimension/continuum have all been used and sometimes interchangeably. Kraeplenian: multiple manifestations of an illness that may change over time.

Distress factor: (Wakefield 1992) this is based onSubthreshold and beyond. threshold syndromal

Reflector of common etiology: e.g. Illness related to basal ganglia (Palumbo et al 1997)

• Series of phenotypic expression of a single diathesis. E.g. the bipolar spectrum as envisaged by Akiskal. • Phenomenologically: on basis of similar symptomatology. E.g. the OC spectrum that has been based on impulsivity, compulsive acts, obsessive thoughts. (Hollander 1994) • Categorical: on basis of a single characteristic e.g. non-psychotic to psychotic mood disorders. • Comorbidity

 clinical course and treatment response. .O-C SPECTRUM DISORDERS • There has been increasing recognition in recent years that a number of clinical psychiatric syndromes may be related to obsessive-compulsive disorder (OCD). these form a distinct category of inter-related disorders referred to as "obsessive-compulsive spectrum disorders.  and often occur comorbidly." • Such disorders and OCD are said to overlap in terms of –  phenomenologic features.  may share a common pathophysiologic basis  and genetic predisposition.

: Body dysmorphic disorder and hypochondriasis. • Compulsive sexual disorders. • Tourette's syndrome and other movement disorders. onchophagia and psychogenic excoriation.: • Impulse-control disorders such as. Recently Included.: • So-called "schizo-obsessive disorders".: • Certain addictive disorders.: • Subsyndromal OCD.: Trichotillomania.: Anorexia and binge eating. pathological gambling. compulsive buying. • Eating disorders such as. . "delusional and schizotypical OCD" and "obsessional schizophrenia.The disorders are the following." Are proposed to be included. meaning OCD that does not cause impairment or distress. Often included are. • Somatoform disorders such as. and repetitive self-mutilation. impulsive personality disorders.

• Initially propounded by • Jenike (1989) who included- – Bowel and Urinary obsessions – Eating disorders – Compulsive gambling – Compulsive sexual behavior – Body dysmorphic disorder – Hypochondriasis – Trichotillomania .


• Cause significant distress and functional impairment. • Poorly diagnosed and inadequately treated. • Often concealed or denied. . • Often overlap or coexist with one another. • They appear to be the source of significant morbidity.• Common and widespread (affecting as much as 10% of the population').

facial shape. Nose size.G. always involve a minor or imagined physical abnormality • Most frequent concerns relate to the face and head (e. Examining the imagined defect in the mirror) • One study showing that as many of one third of its sufferers become housebound .Body Dysmorphic disorder (BDD) • Preoccupation with an imagined or inconsequential defect in physical appearance • Similar to OCD in many respects : recurrent.. by definition. wrinkles or blemishes) • Repeated checking (e..g. skin texture. disturbing and intrusive thoughts • Concerns of BDD.

the overvalued ideas of BDD fall somewhere between obsessions and delusions with respect to how strongly false beliefs are held to be valid. patients with BDD usually are convinced that their irrational preoccupations are justifiable. graphs showing that oneÆs measured head size is within normal limits).• In contrast to OCD. • Thus.. when presented with contradictory evidence (e. a BDD patient will acknowledge that there is no objective support for the concern. • Treatment options : Cognitive therapy  Psychopharmacological treatment ( SSRI’s)  Support groups  Family intervention .g. • However.

and 3) pleasure or relief accompanying the act • Sites most often affected are the scalp.Trichotillomania • Classified as an Impulse Control Disorder 1) recurrent hair pulling. extremities and pubic hair • The behaviour therapy technique (habit reversal) . 2) mounting tension preceding the act. eyelashes. eyebrows.

Tourette's Disorder ( Tourette's Syndrome) • A tic disorder that appears before the age of 18. and often preceded by an unwanted premonitory urge • Individuals describe the need to tic as a buildup of tension. nonrhythmic. • Tics are recurrent physical movements or vocalizations with no apparent cause • Symptoms consist of multiple motor tic (such as twitching for no reason) and vocal tics (such as swearing for no reason) that occur. or energy which they consciously choose to release. as if they "had to do it • Actual tic may be felt as relieving this tension or sensation . although not necessarily at the same time. • Stereotypic. temporarily suppressible. pressure.

Behavioral  Psychological therapies  Relaxation techniques. haloperidol. such as exercise. yoga Typical and atypical neuroleptics including risperidone .• Management of the symptoms of tourette's : Pharmacological. pimozide and fluphenazine Antihypertensive agents clonidine and guanfacine . ziprasidone.

Decreased frontal lobe activity .Compulsive Impulsive Risk avoidance Risk seeking OCD BDD AN Dep Hyp TS Trich Binge eating Comp buying Klep PG SIB Sexcomp BPD ASPD Increased frontal lobe activity (Hollander and Wong 1994) Widely spread around the nosological system.

•Has possible treatment implications. . •Elegant way to conceptualize a series of seemingly unrelated disorders.Need for spectrum concept: •An attractive. fascinating proposition. •Immediately lends itself to a common etiological model.

(Lewis 1936. Hoover 1983. Brown 1942. FAMILY STUDIES • Studies completed prior to 1970’s concluded OCD a family disorder. McKeon. prevalence rates among first degree relatives of OCD probands0. it is necessary to have evidence indicating towards the same • a.To prove a common thread running in all these disorders. Kringlen 1965) • Subsequently borne out.5% (Insel.7-4. Murray 1987) .

Studies that have dealt with OCD in first-degree relatives of patients with OCSDs: • Tic disorders and OCPD occur more frequently in families with h/o OCD (Gradas et al 2001. disruptive behavior . • Monozygotic> dizygotic(52% and 15% respectively) • Pauls and Leckman 1986: greater frequency of OCD in 1st degree relatives of TS patients even in absence of tics. • Certain conditions have particularly strong relationships: • Tourette’s Syndrome • Price et al 1985: 43 twin pairs in which one member had TS found OC symptoms in 83% of the total 86 subjects. Samuels et al 2001) • Relatives of probands with early onset are at a higher risk for both OCD and tics. male gender. • Familial loading for OCD is associated with an early age of onset and is more commonly associated with tics. • Earlier age of onset may be a familial subtype of OCD.

• Lilenfel et al 1998: greater frequency of OCD in relatives of BNP’s.• Eating Disorders: • Halmi et al 1991 and Lilenfeld et al 1998: greater frequency of OCD in 1st degree relatives of patients with AN. • Trichotillomania • Leane et al 1992: increased OCD in relatives • Body dysmorphic disorder • Philips et al 1993: greater frequency of OCD in 1st degree relatives • Kleptomania • Mc Elroy et al 1991: greater frequency of OCD in 1st degree relatives .

 BDD  Grooming disorder  Eating disorder  Hypochondriasis • Were significantly higher in proband’s first degree relatives.Studies that have dealt with OCSDs in firstdegree relatives of patients with OCD: • Pauls et al 1995: relatives of probands with early onset OCD are at higher risk for both OCD and tics. • Bienvenu et al 2000: 80 case probands and 343 firstdegree relatives. .

•    2. “Compulsive” end of spectrum appears more strongly familial. . Evidence for Kleptomania Pathological gambling Pyromania • 3. Studies seem to suggest that early age of onset of OCD is associated more with TS. pathological grooming can be considered familial OCSDs. • 5. has specific symptoms and may reflect a common genetic vulnerability to particular symptoms of OCD and comorbid tics. Familial diathesis seems to exist.• Conclusions: • 1. more strongly familial. • 4. Somatoform disorders such as BDD.

b. • Most commonly • MDD-55% • Social phobia • GAD (Eisen et al 1999) . COMORBIDITY • Relatively common for patients with OCD to be diagnosed with other psychiatric conditions.

To consider OCSD’s – • Studies regarding OCD in patients with OCSDs: • Patients with hypochondriasis (Barsky et al 1992). anorexia nervosa (Halmi et al 1991. Lilenfeld et al 1998). and bulimia nervosa (Keck et al 1990) are associated with elevated life-time risks of OCD. • Uncontrolled clinical series suggest the same for  BDD (Philips et al 1993)  Pathologic skin picking (Arnold et al 1998)  Trichotillomania (Christiensen et al 1991)  Kleptomania (McElroy et al 1991)  Pathological gambling (Linden et al 1986) .

. 67% had a lifetime history of at least one OCSD.6% of 85 subjects with OCD met criteria for OCSDs currently. highest being: Compulsive self injury (22.6%) Intermittent explosive disorder (10. • Eisen and Rasmussen 1993: OCD patients have a higher lifetime prevalence of AN and BN.Studies regarding OCSDs in patients with OCD: • •      Major studies: du Toit et al 2001: 57.4%) Compulsive buying (10.6%) • Sanson et al 1996: OCD patients have more hypochondriacal fears and beliefs.

• OC symptoms are common in patients with schizophrenia. early onset. . single and have a deteriorative course. Out of 475 patients with OCD. Patients with primary OCD show high percentage of tics (7-57%) (Rasmussen et al 1990. Association between tics. Comparing patients with OCD alone and patients with OCD and TS. (Geller et al 2001) 2. 14% had psychotic symptoms. male gender. latter group has been found to more likely to have:  Symmetrical obsessions associated with magical thinking  Fear of doing something embarrassing  Intrusive violent/sexual imagery  Touching compulsions  Self-injurious behavior (George et al 1993) 3. • Tic Disorders: 1. probands of OCD with psychosis are more likely to be male. disruptive behavior has already been described. Miguel et al 1995).

post encephalitis lethargica. • These have been via neurochemical and neuroanatomical findings . NEUROBIOLOGY • There have always been hints to OCSDs being “biological” in origin.c. eg Sydenham’s chorea. • This has been put on a much stronger footing only recently.

Insel 1987) • Later it was also found that CLM is also more effective than DSM in a variety of disorders with STEREOTYPIC MOVEMENTS. Neurochemistry • OCD responds to clomipramine that has a serotonergic action.CPP (serotonergic antagonist) exacerbates OC symptoms • Clomipramine is more effective in OCD than desimipramine that has a NA action.1. (Zohar. • This has included studies done in: – – – – Hair pulling (Swedo et al 1989) Nail biting (Leonard et al 1991) OC symptoms in autism (Gordon et al 1992) BDD (Philips et al 1993) . • m.

it does not indicate a common pathophysiology. just because a certain class of drugs is effective in a range of conditions. • SRI s have been found less effective in  Trichotillomania (Stein et al 1995)  Autism (Gordon et al 1992)  Many cases of OCD are refractory to SSRIs .• This indicates a certain common biochemical substrate in these disorders • On the contrary.

. oxytocin and vasopressin etc are involved in repetitive movement disorder. (McDougle et al 1994) – Tic disorders respond to dopamine blockers and dopamine agonists exacerbate tics. SSRI addition to antipsychotic may help in the response. (Leckman et al 1994) • Conclusions: Serotonin hypothesis is largely an oversimplification. as the facts do not support an exclusive role of serotonin in all of the OCSDs.• Dopamine-serotonin hypothesis – Anti-psychotic augmentation is useful for SSRI resistant OCD especially when it is associated with tics. (Hanbridge et al 1996. (Goodman et al 1990) – In TD as well as trichotillomania. Stein and Hollander 1992) – There is also evidence that systems such as opioidssteroids.

Saxena et al 1998) • Also. Neuroanatomy • Neuroimaging studies related to OCD have suggested:  Abnormal metabolic activity in Orbito-frontal cortex  Anterior cingulate region  Caudate nucleus (Rauch and Baxter 1998. .2. • Cortico-basal ganglia network activity is increased at rest relative to that in controls. • OCD: it is the neural circuits interconnecting Orbito-frontal and anterior cingulate cortex with basal ganglia that is involved.

In other OCSDs: • TD:  Activity in the prefrontal cortex and the caudate nucleus is increased  MRI has also shown abnormalities of BG including putamen in TD. (O’ Sullivan et al 1997) • Thus even though investigators have postulated a “Developmental basal ganglia syndrome” to explain OCSDs. . (Singer et al 1993)  OCD patients in TD show increased metabolism Orbito-frontal cortex and putamen. (Braun et al 1995) • Trichotillomania: Left putamen is smaller than that in controls.

1986) .Behavioral Regulation Through FrontalSubcortical Circuits Frontal Cortex Striatum + Direct Pathway D1 D2 + + GPI & SNr - Indirect Pathway Thalamus GPE + - Subthalamic Nucleus (Alexander et al.

Indirect Basal Ganglia Control System Direct Pathway Indirect Pathway Stimulatory Inhibitory OCD .

• However these divisions are overlapping. • Alexander et al 1990 have postulated different sets of cortico-basal ganglia loops with specializing functions depending upon cortical areas participating in the loops.• Direct pathway: the cortical activation of basal ganglia via the direct pathway results in facilitation of selected motor functions. • Putamen: mainly associated with motor aspects • Nucleus accumbens and caudate nucleus: cognitive and behavioral aspects. • It is postulated that OCD involves an imbalance between these 2 pathways. the differents loops are supposed to explain the phenomenological differences between the different OCSDs. Huntington’s and all Basal Ganglia pathology conditions. . • Indirect pathway: leads to a suppression of unwanted motor behavior. however this explanation has been used to explain conditions as diverse as PD. • In this broad based framework.

Neuroimmunology • Autoimmune basis: • Apparent OC symptoms seen in patients with Sydenham’s chorea and also post-encephalitis lethargica suggest an autoimmune basis. • • • • Sydenham’s chorea: Following GABHS infection Some of the movements resemble tics Significant numbers of patients with Sydenhams chorea meet criteria for OCD and often have tics as well.3. (Swedo and Leonard 1994) • Increased antineuronal antibodies have also been found suggesting an autoimmune process underlying damage to basal ganglia in patients who develop OCD. Leonard. Kiessling 1994) . (Swedo.

Swedo 2001) • D 8/17 (B Lymphocyte antigen) has been found to be significantly higher in children with PANDAS.PANDAS (Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection): • Refers to patients with tics and OC symptoms induced by streptococcal infections. Swedo 2001) . (Leonard. (Swedo et al 1997. Murphy et al 1997) • IMPLICATIONS: • May allow for testing of models of pathogenesis. Sydenhams chorea and childhood onset OCD and TS compared to normal controls. • May suggest antibiotic prophylaxis and therapeutic plasma exchange (encouraging results by Leonard.

are recognized by the patient as excessive or unreasonable . • DSM-IV: OCD diagnostic criteria :• A chronic illness involving either obsessions or compulsions that: Cause marked distress Occupy more than one hour a day Significantly interfere with normal routine.d. INSIGHT.OCD is an illness with insight.occupational (or academic) functioning or usual social activities or relationships At some point during the course of disorder .A SEPARATE SPECTRUM • By definition.

the person does not recognize that the obsessions and compulsions are excessive or unreasonable • Concept: Delusional and non-delusional variants of OCSDs are same rather than different disorders and insight is a dimensional rather than a categorical construct . for most of the time during the current episode.• DSM-IV: Poor Insight Type :Specify if poor insight type: if.

higher frequency of schizophrenia spectrum disorders in family members. (Monte et al 2002) • Patients with OCD and poor insight have been found to have higher severity of OCD symptoms. lack of resistance and poor treatment motivation.• Patients with hoarding showed poor insight. (Yeller et al 1998) . (Catapano et al 2001) • Juvenile OCD has also been found to have poor insight. (Damecour and Charion 1998) • OCD patients with poor insight were relatively more likely to have hoarding and repeating rituals.

Psychiatry Res. Yokohama. . Aoba-ku.Obsessive-compulsive disorder and obsessive-compulsive symptoms in Japanese inpatients with chronic schizophrenia . Epub 2010 May 18.a possible schizophrenic subtype.179(3):241-6. Owashi T.Department of Psychiatry. 2010 Oct 30. which is related to earlier onset and more severe psychotic symptoms. Ota A. Kamijima K. Fujigaoka. Showa University Fujigaoka Hospital. Otsubo T. Japan Our findings suggest there is a subtype of schizophrenia with OCS. Susa Y.

Need to control thoughts and dysfunctional beliefs about the malleability of worries may represent critical prerequisites for the two phenomena to emerge. findings suggest that obsessions and hallucinations may share a common metacognitive pathway. University Medical Center Hamburg Eppendorf.Cogn Neuropsychiatry.15(6):531-48.Department of Psychiatry and Psychotherapy. Epub 2010 May 4. CONCLUSIONS: Notwithstanding large pathogenetic differences between OCD and schizophrenia. 2010 Nov. Hamburg. Lincoln TM. Larøi F. Germany.Moritz S. Peters MJ.Metacognitive beliefs in obsessive-compulsive patients: a comparison with healthy and schizophrenia participants. .

Maj M . The results suggest that the specifier "poor insight" helps to identify a subgroup of patients at the more severe end of OCD spectrum. Cioffi V. and a poorer prognosis. 2010 Obsessive-compulsive disorder with poor insight: a three-year prospective study. De Santis V. received more frequently augmentation with antipsychotics. a diminished response to standard pharmacological interventions.Prog Neuropsychopharmacol Biol Psychiatry. characterized by a more complex clinical presentation. Fabrazzo M. poor insight OCD patients were less likely to achieve at least a partial remission of obsessivecompulsive symptoms. Conclusion : During the follow-up period. Catapano F. Giacco D. . required a significantly greater number of therapeutic trials. Perris F.

2% 25% 7.5% 10% 6.Comorbidity of Schizophrenia and OCD • • • • • • • Muller et al (1953): Rudin et al (1953): Ingram et al (1961): Rasmussen et al (1986): Karno et al (1988): Berman et al (1995): Eisen et al (1997): 12.8% .3% 10% 12.

(2001): (male patients) • Poyurovsky et al (2001): • Ohta et al.5% 18.• Poyurovsky et al (1999): • Tibbo et al. (2003): (adolescents) • Zohar et al (2003): 14% 25% 10% 23. (2003): • Nechmad eAt al.(2000): • Fabisch et al.3% 26% 15% .

Possible models of interaction between schizophrenia and OCD Schiz OCD Comorbidity is an artefact of overlapping diagnostic criteria Schizophrenia and OCD are separate disease entities True comorbidity: two disorders occurring at the same time Schiz OCD Schiz OCD .

expressed in two different phenotypes . with common aetiology.Possible models of interaction between schizophrenia and OCD (2) schiz Schiz- OCD Obess. The mixed schizophrenia and OCD syndrome is a separate entity schiz OCD Schizphrenia predisposes to OCD Common aetiology schiz OCD One entity.



Tasman A. Keck PE Jr. J Am MedWomens Assoc 1994. Eating disorder history in women with obsessive compulsive disorder. • Rasmussen SA. Hertzer J. PhD Department of Psychiatry.Bibliography • Kay J. J Clin Psychiatry 1994.23(7):355-8. University of Ottawa • Hollander E. • McElroy SL. Obsessive-compulsive spectrum disorder. Obsessive compulsive spectrum disorders: i Clin Psychiatry 1994. Psychiatr Ann 1993. Phillips KA. Kaufman R.2006)(T)(1081s) • Obsessive-compulsive spectrum disorders Arun V. MB.55:89-91. Ravindran. Obsessive compulsive spectrum disorders: an overview. . BS.49(1):24-6.55(SuppllO) • Tamburrino MD.. Essentials of Psychiatry (Wiley.

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