The etiology and treatment of developmental stammering in childhood (DS, also called idiopathic stammering or stuttering) are reviewed by a speech pathologist and psychologist at the University of Reading, UK. Prevalence is estimated at 1 to 3% of the population. DS is distinguished from neurogenic stammering (secondary to stroke, tumor, or degenerative disease) and psychogenic stammering. DS usually develops in pre-school age groups, the mean age at onset of 4 years, with 75% cases beginning before age 6. The cause is multifactorial, demands placed on the child exceeding the capacity to manage speech and language variables. The evidence for a genetic component to stammering is strong, twin studies showing concordance in monozygotic twins of 75 - 89%. Some children with DS are linguistically advanced while others are delayed. A mismatch between motor speech and language abilities may cause impairment in fluency, when articulation skills are not sufficiently developed to keep pace with verbal output. Another theory invokes a faulty auditory processing, that may respond to delayed auditory feedback therapy. Neuroimaging in adults who stammer may show hemispheric asymmetries, and neurochemical studies report both increased and decreased levels of dopamine. Risperidone, a D2 antagonist, may reduce severity of stammering in some adults. Treatment recommendations in children vary from an indirect approach, with changes in the child's environment to reduce demands, to direct intervention, targeting speech output and capacity. Complete recovery, with or without therapy, is common before adolescence. Approximately 74% of children who stammer recover, 89% of young females. Boys are affected most frequently; those with a late onset of DS have the poorest prognosis, especially when complicated by speech and language delay. 
COMMENT. Stammering is developmental (idiopathic) or acquired. Particularly in adults, it may be secondary to organic brain disease or of psychogenic origin. In children it is most likely developmental and usually transient, requiring only an adjustment of parental handling or school pressure. If persistent and complicated by seizures or other neurologic manifestations, investigations should include an EEG and MRI. In rare cases, the differential diagnosis may include Landau-Kleffner syndrome; symptoms are associated with an acute onset of loss of speech comprehension and auditory agnosia, seizures and/or a paroxysmal EEG with bitemporal discharges. 
Structural and functional abnormalities of the motor system in developmental stuttering are reported by researchers at the Departments of Experimental Psychology and Clinical Neurology, University of Oxford; and Department of Psychology, University College London, UK . Using functional and diffusion imaging, motor and language areas were examined in brains of 12 young subjects (aged 14-27 years;avg 18 years; 1 left-hander) who stutter. During speech production, people who stutter show overactivity relative to controls in the anterior insula, cerebellum and midbrain bilaterally and underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl's gyrus in the left hemisphere. The overactivity in the midbrain, at the level of the substantia nigra, red and subthalamic nuclei, is consistent with a previous report of excess dopamine in adults who stutter. Areas with underactivity are associated with articulation and speech production, and show loss of white matter. Stuttering is related to disruption in neural systems that support the execution of fluent speech.