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Concept of Spectrum
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
Initially propounded by
Jenike (1989)
who included-
Bowel and Urinary obsessions Eating disorders Compulsive gambling Compulsive sexual behavior Body dysmorphic disorder Hypochondriasis Trichotillomania
OCD
In contrast to OCD, patients with BDD usually are convinced that their irrational preoccupations are justifiable. However, when presented with contradictory evidence (e.g., graphs showing that ones measured head size is within normal limits), a BDD patient will acknowledge that there is no objective support for the concern. Thus, the overvalued ideas of BDD fall somewhere between obsessions and delusions with respect to how strongly false beliefs are held to be valid. Treatment options : Cognitive therapy Psychopharmacological treatment ( SSRIs) Support groups Family intervention
Trichotillomania
Classified as an Impulse Control Disorder 1) recurrent hair pulling, 2) mounting tension preceding the act, and 3) pleasure or relief accompanying the act Sites most often affected are the scalp, eyebrows, eyelashes, extremities and pubic hair The behaviour therapy technique (habit reversal)
Management of the symptoms of tourette's : Pharmacological, Behavioral Psychological therapies Relaxation techniques, such as exercise, yoga Typical and atypical neuroleptics including risperidone , ziprasidone, haloperidol, pimozide and fluphenazine Antihypertensive agents clonidine and guanfacine
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.
An attractive, fascinating proposition. Elegant way to conceptualize a series of seemingly unrelated disorders. Immediately lends itself to a common etiological model. Has possible treatment implications.
To prove a common thread running in all these disorders, it is necessary to have evidence indicating towards the same
a. FAMILY STUDIES Studies completed prior to 1970s concluded OCD a family disorder. (Lewis 1936, Brown 1942,
Kringlen 1965)
Subsequently borne out, prevalence rates among first degree relatives of OCD probands0.7-4.5% (Insel, Hoover 1983; McKeon, 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, Samuels et al 2001) Relatives of probands with early onset are at a higher risk for both OCD and tics. Earlier age of onset may be a familial subtype of OCD. Certain conditions have particularly strong relationships: Tourettes Syndrome Price et al 1985: 43 twin pairs in which one member had TS found OC symptoms in 83% of the total 86 subjects. 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. Familial loading for OCD is associated with an early age of onset and is more commonly associated with tics, male gender, disruptive behavior
Eating Disorders: Halmi et al 1991 and Lilenfeld et al 1998: greater frequency of OCD in 1st degree relatives of patients with AN. Lilenfel et al 1998: greater frequency of OCD in relatives of BNPs. 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
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, BDD Grooming disorder Eating disorder Hypochondriasis Were significantly higher in probands first degree relatives.
Conclusions: 1. Somatoform disorders such as BDD, pathological grooming can be considered familial OCSDs. 2. Evidence for Kleptomania Pathological gambling Pyromania
3. Compulsive end of spectrum appears more strongly familial. 4. Familial diathesis seems to exist. 5. Studies seem to suggest that early age of onset of OCD is associated more with TS, more strongly familial, has specific symptoms and may reflect a common genetic vulnerability to particular symptoms of OCD and comorbid tics.
b. COMORBIDITY
Relatively common for patients with OCD to be diagnosed with other psychiatric conditions. Most commonly MDD-55% Social phobia GAD (Eisen et al 1999)
To consider OCSDs
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)
Sanson et al 1996: OCD patients have more hypochondriacal fears and beliefs.
Eisen and Rasmussen 1993: OCD patients have a higher lifetime prevalence of AN and BN.
OC symptoms are common in patients with schizophrenia. Out of 475 patients with OCD, 14% had psychotic symptoms, probands of OCD with psychosis are more likely to be male, single and have a deteriorative course.
Tic Disorders: 1. Association between tics, male gender, early onset, disruptive behavior has already been described. (Geller et al 2001) 2. Comparing patients with OCD alone and patients with OCD and TS, 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. Patients with primary OCD show high percentage of tics (7-57%) (Rasmussen et al 1990; Miguel et al 1995).
c. NEUROBIOLOGY
There have always been hints to OCSDs being biological in origin, eg Sydenhams chorea, post encephalitis lethargica. This has been put on a much stronger footing only recently. These have been via neurochemical and neuroanatomical findings
1. Neurochemistry
OCD responds to clomipramine that has a serotonergic action. m- CPP (serotonergic antagonist) exacerbates OC symptoms Clomipramine is more effective in OCD than desimipramine that has a NA action. (Zohar, Insel 1987) Later it was also found that CLM is also more effective than DSM in a variety of disorders with STEREOTYPIC MOVEMENTS. 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)
This indicates a certain common biochemical substrate in these disorders On the contrary, just because a certain class of drugs is effective in a range of conditions; it does not indicate a common pathophysiology.
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
Dopamine-serotonin hypothesis
Anti-psychotic augmentation is useful for SSRI resistant OCD especially when it is associated with tics. (McDougle et
al 1994)
Tic disorders respond to dopamine blockers and dopamine agonists exacerbate tics. (Goodman et al 1990) In TD as well as trichotillomania, SSRI addition to antipsychotic may help in the response. (Hanbridge et al 1996,
Stein and Hollander 1992)
There is also evidence that systems such as opioidssteroids, oxytocin and vasopressin etc are involved in repetitive movement disorder. (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.
2. Neuroanatomy
Neuroimaging studies related to OCD have suggested: Abnormal metabolic activity in Orbito-frontal cortex Anterior cingulate region Caudate nucleus (Rauch and Baxter 1998, Saxena et al
1998)
Also, 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. (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. (O Sullivan et al 1997) Thus even though investigators have postulated a Developmental basal ganglia syndrome to explain OCSDs.
+
Direct Pathway
D1
D2
Indirect Pathway
Thalamus
GPE
Direct Pathway
Indirect Pathway
Stimulatory
Inhibitory
OCD
Direct pathway: the cortical activation of basal ganglia via the direct pathway results in facilitation of selected motor functions. Indirect pathway: leads to a suppression of unwanted motor behavior. It is postulated that OCD involves an imbalance between these 2 pathways, however this explanation has been used to explain conditions as diverse as PD, Huntingtons and all Basal Ganglia pathology conditions. Alexander et al 1990 have postulated different sets of cortico-basal ganglia loops with specializing functions depending upon cortical areas participating in the loops. Putamen: mainly associated with motor aspects Nucleus accumbens and caudate nucleus: cognitive and behavioral aspects.
However these divisions are overlapping. In this broad based framework, the differents loops are supposed to explain the phenomenological differences between the different OCSDs.
3. Neuroimmunology
Autoimmune basis: Apparent OC symptoms seen in patients with Sydenhams chorea and also post-encephalitis lethargica suggest an autoimmune basis. Sydenhams 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. (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. (Swedo, Leonard, Kiessling 1994)
DSM-IV: Poor Insight Type :Specify if poor insight type: if, for most of the time during the current episode, 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
Patients with hoarding showed poor insight, lack of resistance and poor treatment motivation.
(Damecour and Charion 1998)
OCD patients with poor insight were relatively more likely to have hoarding and repeating rituals. (Monte et al 2002) Patients with OCD and poor insight have been found to have higher severity of OCD symptoms, higher frequency of schizophrenia spectrum disorders in family members. (Catapano et al 2001) Juvenile OCD has also been found to have poor insight. (Yeller et al 1998)
Psychiatry Res. 2010 Oct 30;179(3):241-6. Epub 2010 May 18.Obsessive-compulsive disorder and obsessive-compulsive symptoms in Japanese inpatients with chronic schizophrenia - a possible schizophrenic subtype. Owashi T, Ota A, Otsubo T, Susa Y, Kamijima K.Department of Psychiatry, Showa University Fujigaoka Hospital, Fujigaoka, Aoba-ku, Yokohama, Japan
Our findings suggest there is a subtype of schizophrenia with OCS, which is related to earlier onset and more severe psychotic symptoms.
Cogn Neuropsychiatry. 2010 Nov;15(6):531-48. Epub 2010 May 4.Metacognitive beliefs in obsessive-compulsive patients: a comparison with healthy and schizophrenia participants.Moritz S, Peters MJ, Lari F, Lincoln TM.Department of Psychiatry and Psychotherapy, University Medical Center Hamburg Eppendorf, Hamburg, Germany.
CONCLUSIONS: Notwithstanding large pathogenetic differences between OCD and schizophrenia, findings suggest that obsessions and hallucinations may share a common metacognitive pathway. Need to control thoughts and dysfunctional beliefs about the malleability of worries may represent critical prerequisites for the two phenomena to emerge.
Prog Neuropsychopharmacol Biol Psychiatry. 2010 Obsessive-compulsive disorder with poor insight: a three-year prospective study. Catapano F, Perris F, Fabrazzo M, Cioffi V, Giacco D, De Santis V, Maj M
Conclusion : During the follow-up period, poor insight OCD patients were less likely to achieve at least a partial remission of obsessivecompulsive symptoms; required a significantly greater number of therapeutic trials; received more frequently augmentation with antipsychotics. The results suggest that the specifier "poor insight" helps to identify a subgroup of patients at the more severe end of OCD spectrum, characterized by a more complex clinical presentation, a diminished response to standard pharmacological interventions, and a poorer prognosis.
Poyurovsky et al (1999): Tibbo et al.(2000): Fabisch et al.(2001): (male patients) Poyurovsky et al (2001): Ohta et al. (2003): Nechmad eAt al. (2003): (adolescents) Zohar et al (2003):
Schiz OCD
Schiz
OCD
OCD Obess.
schiz
OCD
Common aetiology
schiz OCD
Bibliography
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