Treatment for the management of Obsessive-Compulsive Disorder in Children: A Review

Uday Gaikwad* and Milind Parle

Pharmacology Division, Dept. Pharm. Sciences, Guru Jambheshwar University of Science and Technology,  Post Box-38, Hisar-125 001, Haryana, India

*Corresponding Author E-mail:  uduraj2003@gmail.com

 

ABSTRACT:

Obsessive-Compulsive Disorder (OCD) is characterized by absurd, recurrent and persistent thoughts (obsessions) followed by certain stereotyped actions (compulsions). Obsessive-Compulsive disorder can impair all areas of brain functioning and produce devastating effects on patients and their families. Therefore, there is necessity to aware about the OCD in children and different treatments for its management. The Group A Beta–Hemolytic Streptococcal (GABHS) infections produce antineuronal antibodies that adversely affect basal ganglia cells might play part in etiology of OCD in children. As a result of obsessions, (usually obsessions concerning dirt and contamination, or fear of harming others), many children with OCD develop an avoidant behavior. The newer generation of antidepressant drugs viz. fluvoxamine, fluoxetine, paroxetine, sertraline and citalopram have also been found useful in management of OCD. Neurosurgical treatments have been used for the management of chronic, severely distressing forms of OCD where conventional treatments are ineffective. Psychopharmacological treatments have also been found useful in reduction of repetitive unpleasant behavior. Pharmacological and psychopharmacological treatments combinely have been providing strong effective management of in vivo serotonin impairment as well as reduction of repetitive unpleasant behavior which account for characteristics of OCD.

 

KEYWORDS: Obsession, Compulsion, Antidepressant, Psycho treatment

 

 


 

INTRODUCTION:

Many children with obsessive-compulsive disorder (OCD) suffer from an almost pathological doubting, which can vary from a mild form to an incapacitating form of extreme severity, in which the child is uncertain about its own understandings. Other high frequency symptoms are checking, fear of harming others, obsessions relating to death or sex produce compulsions serving to avoid a horrible event. Indecisiveness is frequently found in children with OCD and ranges from difficulty in making minor decisions. Following Group A Beta–Hemolytic Streptococcal (GABHS) infections, it was noted that OCD symptoms along with choreic movements in sydenham chorea became worse, and this was mediated by antineuronal antibodies that adversely affected basal ganglia cells. It was later hypothesized that this abnormal reaction to GABHS might play a part in the etiology of OCD.1 This subgroup of OCD patients has been termed PANDAS (for Pediatric Autoimmune Neuropsychiatric disorders Associated with Streptococcal Infection). Asbahr, Ramos, Negrao and Gentil presented four cases of children with PANDAS.

 

They suggested that OCD may occur after repeated streptococcal infection as all four cases developed OCD only after the second infection.  MRI tests showed that children with PANDAS have enlarged basal ganglia. The frontal-lobe function compared in 21 children and adolescents with OCD who were approximately 12 years of age and in matched healthy subjects, investigators found no cognitive impairment on the basis of performance on frontal tests and concluded that OCD symptoms may not interfere with cognitive abilities at early stages in the illness. The study with 42 children and adolescents (mean age, 14 years) and 35 normal subjects and concluded that subjects with OCD have impaired executive functions and nonverbal memory. Andres administered a neuropsychological battery to 35 OCD patients without psychiatric comorbidity aged between 7 and 18 years and 35 healthy controls and found that children and adolescents with OCD had impairments in visual memory, visual organization.2

 

The performances of 21 obsessive-compulsive children compared with 21 healthy controls on neuropsychological tests, including the Stroop test, Wisconsin Card Sorting Test, Verbal Fluency test, California Verbal Learning Test, Grooved Pegboard Test suggested there were no differences in neuropsychological performance between obsessive-compulsive children and the healthy controls. Therefore, it was concluded that obsessive-compulsive children do not show clinically significant cognitive impairment during the early stages of the illness, but a deficiency may become significant over time. The doubting and checking are found frequently in OCD patients who associated with memory dysfunction of OCD patients. The children with tic disorder frequently show OCD symptoms. The negative emotions such as anxiety have an adverse effect on memory function. The most striking feature of the symptoms presented by obsessive-compulsive children is the severity of the psychopathology in the absence of formal thought disorder. Thus, Obsessive-Compulsive disorder can impair all areas of brain functioning and produce devastating effects on patients and their families. Therefore, there is necessity to aware about the OCD in children and different treatments for it’s management.

 

EPIDEMIOLOGY:

The frequency of compulsions in 8-year-old German children, to be 4.6% (moderate severity) and 2.8% (severe symptomatology).3 Later, the prevalence of compulsive checking in the same population (13 years old) was 3.4%, all of moderate severity. 2.3% reported compulsion for cleanliness and 4.0% experienced obsessive thoughts. OCD in the child psychiatric population found as 0.2-1.2%.4 In an epidemiological study of 5000 high-school students, Flament found that 0.35% fulfilled the criteria of OCD, as defined by DSM-III (American Psychiatric Association, 1980).5 They calculated a lifetime prevalence of 0.4%. In their Isle of Wight-study, 2000 children examined at the age of 11 and found no children who fulfilled the criteria for OCD.6 They found eight children whom they diagnosed with "mixed emotional disorder" (with obsessive-compulsive features).

 

FAMILY LIFESTYLE AND GENETICS:

Family lifestyle could be regarded as a possible precipitating factor, for developing obsessive-compulsive symptoms in predisposed children. Family functioning was described in 20 Danish children with OCD and later assessed adaptability and cohesion of the family.7 In studies of children and adolescents most surveys show that OCD patients are generally from white, middle- or upper-class, intact families. Certain myths have prevailed regarding families with OCD children. The families are often said to show a cultural behaviour that emphasises cleanliness and perfection. 9% of mothers and 25% of fathers to OCD children had OCD themselves. 19% of 21 OCD children had one parent with OCD and as many as 52% had parents with obsessive-compulsive symptoms, without meeting the criteria for OCD, when parents were interviewed with standard clinical psychiatric assessments. 52% of children with OCD have a positive family history of OCD amongst first-degree relatives and that risk to relatives is related to the age of onset of the OCD proband: the younger the onset of OCD in proband, the higher risk of OCD or Tourette's syndrome in relatives.8 24% of referred OCD children had a first degree relative with OCD.

 

BIOLOGICAL ASPECTS:

An electrophysiological investigation in obsessional states informed the presence of altered neural inhibition in connection with obsessive symptoms. The EEGs of a group of OCD patients compared with a control group of patients with other neurotic disorders, indicated abnormal findings in two thirds of the OCD patients, which was not significantly higher than in the control group.9 An orbitofrontal-subcortical hyperactivity in children and adolescent OCD patients may be the result of abnormal neuroanatomical development of these structures. A report suggested OCD develop by head injuries in four cases.10 The OCD patients have a particularly higher range of neurological diseases in childhood.

 

NEUROLOGICAL SOFT-SIGNS AND NEUROPSYCHOLOGICAL FINDINGS:

Soft-signs are non-localized deviant performances in a motor or sensory test, without other signs or presence of focal neurological disorder. Soft-signs in child psychiatric patients have been well studied and implications of soft-signs have been thouroughly analysed in a general population of pre-school and school-children.11 44 out of 54 childhood OCD patients, at the age from 6 to 20 years, had neurological abnormalities. Of these 44 patients 18 had choreiform movements, 13 had non-specific neurodevelopmental signs only, eight had left hemisyndrome, and five had miscellaneous abnormalities. Most studies conducted on OCD children have resulted an overweigth of soft-signs, compared to normal control-groups. The children with early OCD onset, have more soft-signs than children with a later onset. The neurological soft-signs found in 18.6% of 61 OCD-children and adolescents compared to 14.4% in a control group consisting of non-psychotic and non-retarded children and adolescents with psychiatric disorders other than OCD. In studies of children, a pattern of association between OCD and selected neurological disorders has been long recognized. A prominently left frontal dysfunction in OCD patients indicated that cerebral cause had responsible for the obsessive-compulsive symptoms.

 

TREATMENT OF OCD:

Pharmacological treatments:

The serotonin reuptake inhibitors (SRIs) are consistently effective in patients of Obsessive-compulsive disorder. The anti-obsessional effects of potent SRIs produce progressive desensitization of the presynaptic autoreceptors present on 5HT neurons and their nerve terminals, thereby increasing synaptic 5HT release in the orbitofrontal cortex. Clomipramine was the first to show beneficial effects on OCD symptoms. The newer generation of antidepressant drugs viz. fluvoxamine, fluoxetine, paroxetine, sertraline and citalopram have also been found useful in management of OCD. The mean daily dosage is 50–200 mg for sertraline, 20–80 mg for fluoxetine, 40–60 mg for paroxetine and 150–300 mg for fluvoxamine. The atypical antipsychotics such as risperidone act as new therapeutic options for refractory OCD. Gaikwad et al., 2007 suggested that LHRH agonist such as leuprolide may be clinically effective in OCD, resulted dose dependently attenuated marble-burying behavior in mice has been used to model anxiety disorders viz. obsessive–compulsive disorder.12

 

Neurosurgical treatments:

Neurosurgical treatments have been used for the management of chronic, severely distressing forms of OCD where conventional treatments are ineffective. In the United States and Canada, anterior cingulotomy was the most widely used neurosurgical procedure applied in the treatment of anxiety refractory OCD. Two surgical techniques have been used: radiofrequency thermolesion or thermocapsulotomy and the newer radiosurgical or gamma knife capsulotomy techniques.13 It has been shown that 50–70% of patients with OCD respond favorably to this type of operation at the end of the follow-up period ranging from 1 to 9 years.14 The Bilateral thermolesions are produced by radiofrequency in the anterior cingulate cortex (ACC) (Broadman areas 24 and 32). It has found that 25% of patients with OCD were slightly improved, 31.3% were markedly improved, 12.5% were functionally normal on medication or psychotherapy maintenance and 12.5% were essentially well without any treatment at the mean follow-up of 9 years. The Y-BOCS used for assessment of OCD symptom severity, resulted a moderate-to-marked improvement (defined as a 50% or greater reduction in Y-BOCS scores) in 57% of cases at the mean 13-year follow-up. Approximately 50–70% of patients with OCD showed good outcome by surgery, indicated no or mild residual symptoms at the follow-up ranging from 16 months to 8 years. The recent report suggested that good outcome was observed in only 33% of cases within 1 year of surgery.15 In the United Kingdom limbic leucotomy was developed, a technique based on making bilateral lesions of the cingulotomy, in addition to those of the original subcaudate tractotomy.

 

Psychological treatments:

Psychological treatments based on cognition-behavioral therapy (CBT) are effective in the treatment of OCD, alone or in combination with SRIs. The current procedures are in vivo (real-life) exposure with self-imposed response prevention (EX/RP) which showed beneficial effects of this behavioral approach in two patients with severely disabling OCD. The reduction in OCD symptom severity was found after 3–7 weeks of EX/RP treatment while no change occurred during the control condition. The goal of CBT treatment is to learn to respond appropriately to intrusive thoughts and urges of OCD in new and much more adaptive ways and to reattribute the belief about “false brain messages” as intimately due to a biomedical disease state. The therapeutic effects showed the functional changes in interactions between the limbic cortex (including the orbital cortex and anterior cingulate gyrus) and the basal ganglia that are extremely important in redirecting information flow toward the integration of new behaviorally significant environmental events during learning. This function may be central in the acquisition of more adapted patterns of behavioral responses during the course of CBT.

 

CONCLUDING REMARKS:

OCD is an anxiety disorder featuring intrusive and troubling thoughts which are perceived as the products of one’s own mind unlike schizophrenia. The Group A Beta–Hemolytic Streptococcal (GABHS) infections produce antineuronal antibodies that adversely affect basal ganglia cells might play part in etiology of OCD in children. As a result of obsessions, (usually obsessions concerning dirt and contamination, or fear of harming others), many children with OCD develop an avoidant behavior and can not participate in leisure activities. Pharmacological and psychopharmacological treatments combinely have been providing strong effective management of in vivo serotonin impairment as well as reduction of repetitive unpleasant behavior, which account for characteristics of OCD.

 

REFERENCES:

1.        Swedo SE, Leonard HL and Garvey M. Pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections: clinical description of the first 50 cases. Am J Psychiat. 1998; 155: 264-271.

2.        Andres S et al. Neuropsychological performance in children and adolescents with obsessive-compulsive disorder and influence of clinical variables. Biol Psychiat. 2007; 61(8): 946-51.

3.        Esser G, Schmidt MH and Woerner W. Epidemiology and course of psychiatric               disorders in school-age children. Results of a longitudinal study. J Child Psychol   Psychiat. 1990; 31: 243-263.

4.        Judd L. Obsessive compulsive neurosis in children. Arch  Gen Psychiat. 1965; 12: 136-143.

5.        Flament MF, Whitaker A and Rapoport JL. Obsessive compulsive disorder in adolescence. An epidemiological study. J American Acad of Child and Adolescence Psychiat. 1988; 27: 764-771.

6.        Rutter M et al. Research report: Isle of Wight studies 1964-1974. Psychol Med. 1976; 6: 313-332.

7.        Thomsen PH. Obsessive-compulsive disorder in children and adolescents. A study of phenomenology and family functioning in 20 Danish cases. European Child and Adolescent Psychiat. 1994; 3: 29-36.

8.        Pauls DL, Goodman WK, Rasmussen,S, Alsobrook JP. Familial risk of obsessive-compulsive disorder. Presented at First International OCD Conference Italy, 1993.

9.        Knolker U. EEG-Frequenzanalysen bei Kindem und Jugendhchen mit               Zwangsneurosen. Zeit schrifft Kinder und Jugendpsychiatrie. 1988; 16: 180-185.

10.     McKeon J, McGuffin P, Robinson P. Obsessive-compulsive neurosis following head injury. A report of four cases. Brit J Psychiat. 1984; 144: 190-192.

11.     Gillberg C. Perceptual, motor and attentional deficits in Swedish primary school              children. Some child psychiatric aspects. J Child Psychol Psychiat. 1983; 24: 377-403.

12.     Gaikwad U et al. LHRH antagonist attenuates the            effect of fluoxetine on             marble-burying behavior in mice. Eur J Pharmacol. 2007; 563: 155-159.

13.     Greenberg BD et al. Neurosurgery for intractable obsessive–compulsive disorder and depression: critical issues. Neurosurg Clin N Am. 2003; 14: 199–212.

14.     Mindus P, Rasmussen SA and Lindquist C. Neurosurgical treatment for refractory obsessive–compulsive disorder: implications for understanding frontal lobe function. J Neuropsychiat Clin Neurosci. 1994; 6: 467–477.

15.     Hodgkiss AD et al. Outcome after the psychosurgical operation of stereotactic               subcaudate tractotomy, 1979–1991. J Neuropsychiat Clin Neurosci. 1995; 7: 230–234.

 

 

 

 

 

 

Received on 12.10.2009          Modified on 30.11.2009

Accepted on 22.12.2009         © RJPT All right reserved

Research J. Pharm. and Tech. 3(1): Jan.-Mar. 2010; Page 66-68