DSM-IV-TR Diagnostic Criteria
Consistent failure to speak in specific social situations (in which there is an expectation of speaking, e.g., at school) despite speaking in other situations.
The disturbance interferes with educational or occupational achievement or with other social communication.
The duration of the disturbance is at least 1 month (not limited to the first month of school).
The failure to speak is not due to a lack of knowledge of, or comfort with, the spoken language required in the social situation.
The disturbance is not better accounted for by a communication disorder (e.g., stuttering) and does not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder.
(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th edn., Text Revision. Copyright 2000, Washington, DC: American Psychiatric Association.)
Selective mutism is more common in girls than boys. Prevalence estimates have varied from 0.08% to 0.7%.
The cause of selective mutism is probably multifactorial. Four types of the disorder have been postulated. In symbiotic mutism, the child manipulates the environment, using shyness and clinging to avoid separation. In passive-aggressive mutism, a child scapegoated by his or her peers trenchantly refuses to speak when called on to do so. Reactive mutism is precipitated by a stressor such as illness, separation, or abuse. In speech phobic mutism, the child is afraid to hear his or her own voice.
Shyness, taciturnity and selective mutism run in families. Selective mutism may be a form of social anxiety. One study found a high prevalence of comorbid social phobia, avoidant personality disorder, and simple phobia in this condition, along with a familial aggregation of social phobia and selective mutism. Some studies suggest that selective mutism may be associated with subtle expressive language impairment.
Like other many other neurodevelopmental disorders of childhood onset, it is likely that there are multiple vulnerability genes associated with this condition.
The age at onset of selective mutism is 1–5 years (average, 2.7 years). Children with selective mutism are most reluctant to speak at school, away from home, to adults, and to unfamiliar people. They are more likely to speak to peers than to teachers. One study found that 13% of children with selective mutism had a learning disorder and 10% had a history of delayed language development, but all had normal speech and language by 5 years of age. No clear association has been found between trauma and the onset of selective mutism, nor has the often-reported association with oppositional behavior been corroborated. Selective mutism may be regarded more appropriately as a symptom of social anxiety, akin to the “freezing” that some adults with social phobia experience when called on to speak in public.
See remainder of this Chapter.
Complications/Adverse Outcomes of Treatment
See remainder of this Chapter.
See remainder of this Chapter.
Black B,Uhde TW: Psychiatric characteristics of children with selective mutism. J Am Acad Child Adolesc Psychiatry
Krysonski VL: A brief review of selective mutism literature. J Psychol 2003;137:29–40.
Steinhausen HC,Wachter M,Laimbock K,Metzke CW: A long-term outcome study of selective mutism in childhood. J Child Psychol Psychiatry
Differential Diagnosis (Including Comorbid Conditions)
SAD and school refusal are most likely to be confused with physical disorders when they have salient somatic anxiety equivalents. Thus gastrointestinal symptoms can be confused with peptic ulcer, esophageal reflux, abdominal emergency, or disorders associated with bowel hurry. SAD with school refusal can also masquerade as chronic fatigue syndrome, chronic muscular pain, and prolonged convalescence from infectious mononucleosis. In panic disorder, mitral valve prolapse should be investigated only if auscultation indicates the need to do so.
Selective mutism should be differentiated from deafness, mental retardation, developmental language disorder, aphonia, and the lack of understanding of a secondary language by recent immigrants. Panic disorder should be distinguished from substance-induced anxiety disorder (e.g., caffeinism), posttraumatic stress disorder, and medical disorders that cause anxiety (e.g., pheochromocytoma).
See Table 41–1 for the general and specific standard interviews and questionnaires useful in screening for and diagnosing anxiety disorders and phobias and in monitoring the treatment outcome of these disorders.
Table 41–1. Psychological Testing for Anxiety Disorders |Favorite Table|Download (.pdf)
Table 41–1. Psychological Testing for Anxiety Disorders
Schedule for Affective Disorders and Schizophrenia in School-Aged Children (K-SADS) (Puig-Antich and Chambers 1978)
Anxiety Disorders Interview for Children (ADIS-C) (Silverman and Nellis 1988)
Diagnostic Interview Schedule for Children (DISC) (Costello et al. 1985)
Revised Children's Manifest Anxiety Scale (RCMAS) (Reynolds and Richman 1978)
Revised Fear Survey Schedule for Children (FSSC-R) (Ollendick 1983)
Multidimensional Anxiety Scale for Children (MASC) (March et al. 1994)
Anxiety disorders (particularly SAD) and depressive disorders frequently coincide. Anxiety disorders are also often encountered in children who have Attention-deficit hyperactivity disorder. Many children with one type of anxiety disorder have at least one other anxiety disorder (e.g., SAD with panic disorder, GAD, or avoidant personality disorder). The high degree of comorbidity may be explained on the basis of a risk hypothesis, on the basis of a hypothesis that there is a single underlying pathogenesis, or on the assumption that the symptoms of anxiety and depression overlap in a dimensional, noncategorical manner.
Curry JF,Murphy LB: Comorbidity of anxiety disorders. In: March J (ed).Anxiety Disorders in Children and Adolescents. New York: Guilford Press, 1995, pp. 301–320.
Obsessive–compulsive disorder is the only anxiety disorder for which a best treatment can be recommended (see Chapter 24). With other anxiety disorders and phobias, it is reasonable to start with behavioral treatments and to try medication only if such treatments are unsuccessful. Family therapy, individual psychotherapy for unresolved conflict, and liaison with the patient's school are also commonly required.
The behavioral techniques most often used are systematic desensitization and exposure, operant conditioning, modeling, and cognitive-behavioral therapy (see Chapter 10).
Selective serotonin reuptake inhibitors (fluoxetine, fluvoxamine, paroxetine, and sertraline), the mixed serotonin and norepinephrine reuptake inhibitor (venlafaxine), tricyclic antidepressants and high-potency benzodiazepines (e.g., alprazolam, clonazepam) hold some promise in the treatment of anxiety disorders. Fluoxetine has been recommended for the treatment of social phobia. In non-OCD anxiety disorders in the pediatric age group involving more than 1,100 patients, the overall response rate was 69% (95% CI, 65–73%) in antidepressant-treated participants versus 39% (95% CI, 35–43%) in those receiving placebo. Four placebo-controlled studies have examined the effectiveness of tricyclic antidepressants in the treatment of SAD. In only one of these studies was the experimental drug more effective than placebo. One controlled study of the effectiveness of clonazepam in treating SAD showed no superiority over placebo. Controlled trials of clonazepam in treating GAD and social phobia showed no superiority over placebo. Fluvoxamine has shown superiority to placebo in the treatment of social phobia, GAD and SAD. There are no controlled studies of the effectiveness of medication in the treatment of juvenile panic disorder. β-Blockers have shown promise in the alleviation of examination performance anxiety in undergraduate students.
Bridge JA,Iyengar S,Salary CB, et al.: Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: A meta-analysis of randomized controlled trials. JAMA
Thienemann M: Medications for pediatric anxiety. In: Steiner H (ed).Handbook of Mental Health Interventions in Children and Adolescents. San Francisco, CA: Jossey Bass, 2004, pp. 288–319.
Walkup JT,Labellarte MJ,Riddle MA et al.: Fluvoxamine for the treatment of anxiety disorders in children and adolescents. N Engl J Med, 2001;344:1279–1285.
Complications/Adverse Outcomes of Treatment
The choice of treatment should be the result of a collaborative discussion between clinician, family, and patient. Presentation of data concerning age-specific benefits should allow for an informed evaluation of the potential benefits and risks of various treatments vs. no treatment and provide a framework for the comparison of drug vs. non-drug treatments.
The predominant adverse effects of antidepressants involve either central nervous system or the gastrointestinal tract. Central nervous system side effects include headache, nervousness, insomnia, drowsiness, anxiety, dizziness, fatigue, sedation, somnolence, mania, hypomania, and irritability. Selective serotonin reuptake inhibitors-associated behavioral activation (i.e., restlessness, hyperkinesis, hyperactivity, agitation) is 2–3-fold more prevalent in children compared to adolescents; it is more prevalent in adolescents compared to adults. Other side effects include sexual dysfunction in adolescent subjects.
The U. S. Food and Drug Administration as well as British and European regulators have issued public health advisories concerning the risk of suicide and self-harm associated with the use of antidepressant medication in the pediatric population. The magnitude of this risk is small, with these medications creating a 2-fold (4% vs. 2%) increased risk for “suicidal behavior or suicidal ideation.” There is a need for close monitoring. Recommended monitoring includes daily observation by caregivers, at least weekly face-to-face visits with patients or their family members or caregivers during the first 4 weeks of treatment, then every other week visits for the next 4 weeks, then at 12 weeks, and then as clinically indicated beyond 12 weeks. In addition, patients should also be monitored for associated behaviors (e.g., anxiety, agitation, panic attacks, insomnia, irritability, aggressiveness, impulsivity, akathisia, hypomania, mania). It is also clear that there is relatively little systematic data concerning the risks associated with the long-term use of these medications especially in young children.
The onset of SAD may be acute and precipitated by stress, or it may be gradual, without apparent precipitant. The prognosis is variable. Some children recover completely; others experience chronic or recurrent separation anxiety. These children are likely to relapse when their attachment relationships are threatened, even into maturity. Children with SAD are likely to develop panic disorder, agoraphobia, or depressive disorders in adolescence or adulthood.
The natural history of GAD is not understood. One study has shown that 65% of children diagnosed as having GAD or phobic disorder no longer carry the diagnosis after 2 years. Social phobia in childhood may become associated with alcohol abuse in adolescence. Most children with selective mutism “outgrow” it within a year of onset, although there may be residual shyness. In a minority of cases, mutism continues into late childhood or adolescence.