By definition, children with a communication diagnosis of motor speech disorder have brain dysgenesis or have sustained pre-, peri-, or postnatal damage or disease to the central or peripheral nervous system or to muscle tissue that impairs control of speech production processes and subsequent actions of the muscle groups used to speak (respiratory, laryngeal, velopharyngeal, jaw, lip, and tongue) (Hodge and Wellman, 1999). This impairment may manifest with one or more of the following: weakness, tone alterations (hypertonia, hypotonia), reduced endurance and coordination, and involuntary movements of affected speech muscle groups (dysarthria), or as difficulty in positioning muscle groups and sequencing their actions to produce speech that cannot be explained by muscle weakness and tone abnormalities (apraxia of speech). Disturbances affecting higher mental processes of speech motor planning and programming underlie the motor speech diagnosis, apraxia of speech. To date, apraxia of speech of known origin in childhood is rare. Conditions in which it may appear are seizure disorders (e.g., Landau-Kleffner syndrome; Love and Webb, 2001), focal ischemic events (Murdoch, Ozanne, and Cross, 1990), and traumatic brain injury. In these cases the speech apraxia is typically accompanied by expressive and receptive language deficits. Oropharyngeal apraxia and mutism have been reported following posterior fossa tumor resection in children (Dailey and McKhann, 1995). Depending on the severity and duration of the neurological insult, signs of childhood-acquired apraxia of speech remit and may disappear.

Disturbances affecting the execution of speech actions are diagnosed as dysarthrias, with subtypes identified by site of lesion, accompanying pathophysiological signs, and effects on speech production. Dysarthrias are the more common type of childhood motor speech disorder. A known neurological condition affecting neuromuscular function, including that of muscles used in speech, is a key factor leading to the diagnosis of dysarthria. A useful taxonomy of subtypes of childhood dysarthrias (with associated sites of lesion) was described by Love (2000) and includes spastic (upper motor neuron), dyskinetic (basal ganglia control circuit), ataxic (cerebellar control circuit), flaccid (lower motor neuron and associated muscle fibers), and mixed (two or more sites in the previous categories); the mixed type is the most common.

Limited research has been published on the nature of neuromuscular impairment in the various childhood dysarthrias and how this correlates with perceived speech abnormalities (Workinger and Kent, 1991). Solomon and Charron (1998) reviewed the literature on speech breathing in children with cerebral palsy. Love (2000) summarized the literature on respiratory, laryngeal, velopharyngeal, tongue, jaw, and lip impairment in children with dysarthria. It is difficult to generalize from the literature to individual cases because of the relatively small numbers of children studied and the range of individual differences in children with neurogenic conditions, even when they share the same neurological diagnosis. Furthermore, it cannot be assumed that because a neurological diagnosis has implicated a certain site of lesion (e.g., cranial nerve or muscle group), other muscle groups are not also impaired. Murdoch, Johnson, and Theodoros (1997) described the case of a child with Möbius syndrome (commonly held to result from damage to cranial nerves VI and VII) and also identified impaired function at the level of the velopharyngeal, laryngeal, and respiratory subsystems using perceptual and instrumental evaluation. However, a reduction in maximal range of performance of speech muscle groups, persistent dependencies between muscle groups (e.g., lip with jaw, jaw with tongue, tongue body with tongue tip), and reductions in speed, precision, and consistency of speech movements are common themes in the literature on the nature of impairment in childhood motor speech disorders.

The effects of most childhood motor speech disorders are to reduce the rate and quality of affected children's speech development, frequency of speech use, speech intelligibility, speaking rate, and overall speech acceptability. The speech disorder can range from mild to so severe that the child never gains sufficient control over speech muscles to produce voice or recognizable speech sounds. These children's psychosocial development is also at risk because of limitations imposed by the speech disorder on social interactions, which in turn may limit their academic progress because of fewer opportunities to gain experience using language (Hodge and Wellman, 1999).

When the cause of a childhood motor speech disorder is known, it is typically because a physician specializing in pediatric neurology has diagnosed it. If this neurological diagnosis (e.g., cerebral palsy, Möbius syndrome, muscular dystrophy) is made during the prelinguistic period, there is some expectation that if neuromuscular dysfunction was observed in earlier nonspeech activities (e.g., sucking, chewing, swallowing, control of saliva, facial expressions) of muscle groups that are involved in speech production, speech development will also be delayed and disrupted (Love, 2000). Congenital suprabulbar paresis, or Worster-Drought syndrome, which has been classified by Clark et al. (2000) as a mild spastic quadriplegic type of cerebral palsy resulting from damage to the perisylvian areas of the cortex, often is not diagnosed until the child is older, if at all. Early diagnosis of this condition is important to speech-language pathologists (Crary, 1993; Clark et al., 2000) because it is predominantly characterized by persisting signs of abnormal neuromuscular dysfunction in oropharyngeal muscles during infants' feeding and swallowing and later control of speech movements. Closer examination of children with congenital suprabulbar paresis also reveals evidence of persisting neuromuscular abnormalities affecting gross and fine motor development and learning difficulties. These children need coordinated, multidisciplinary services like those afforded children with other subtypes of cerebral palsy.

In other cases of childhood motor speech disorders, no abnormal neurological signs are observed in the child's early development, and signs of the motor speech disorder may be the first or only indication of neurological abnormality (Arvedson and Simon, 1998). In some of these cases, subsequent neurological investigation with electromyography, electroencephalography, neural imaging procedures such as magnetic resonance imaging, and metabolic testing identifies a neurological condition or lesion as the cause of the speech disturbance (e.g., seizures and brain dysmorphology in the bilateral perisylvian region, infection, tumor, progressive conditions such as facioscapulohumeral muscular dystrophy) (Hodge and Wellman, 1999). In rare cases, a motor speech disorder may result from treatment for another medical condition, such as surgery for cerebellar tumors or drug treatment for a debilitating movement disorder such as Tourette's syndrome. In still other cases neurological investigation reveals no identifiable cause.

Many conditions that result in childhood motor speech disorders (e.g., cerebral palsy, traumatic brain injury, chromosomal abnormalities) also affect other areas of brain function. Therefore, children may show a mixed dysarthria or characteristics of both dysarthria and apraxia of speech, and they have a high probability of comorbidities affecting higher cognitive functions of language, thought, attention, and memory, sensory-perceptual processes and control of other motor systems (e.g., eyes, limbs, trunk, head).

Multidisciplinary assessment by members of a pediatric rehabilitation team is accepted clinical practice to determine the presence and severity of comorbid conditions that may negatively affect the child's development. Specific to the motor speech disorder, assessment goals may include one or more of the following: establishing a differential diagnosis; identifying the nature and severity of impaired movement control in each of the muscle groups used to produce speech; describing the nature and extent of limitations imposed by the impairment on the child's speech function in terms of articulatory adequacy, prosody and voice, and speech intelligibility, quality, and rate; determining the child's ability to use speech, together with other modes, to communicate with others in various contexts of daily life; and making decisions about appropriate short-and long-term management (Hodge and Wellman, 1999; Yorkston et al., 1999; Love, 2000). At young ages or in severe cases, making a differential diagnosis can be difficult if the child has insufficient speech behaviors to analyze and lacks the attentional, memory, and cognitive abilities to execute tasks that are classically used to differentiate dysarthria from praxis disturbances. Hodge (1991) summarized strategies for assessing speech motor function in children 0–3 years old. Love and Webb (2001) reviewed primitive and oropharyngeal reflexes that may signal abnormal motor development at young ages. Hayden and Square (1999) developed a standardized, normed protocol to aid in the systematic assessment of neuromotor integrity of the motor speech system at rest and when engaged in vegetative and volitional nonspeech and speech tasks for children ages 3–12 years. Their protocol was designed to identify and differentially diagnose childhood motor speech disorders and is built on their seven-stage hierarchical model of speech motor development and control. Thoonen et al. (1999) described the use of several maximal performance tasks (diadochokinetic rates for repeated mono-and trisyllables, sustained vowel and fricatives) in a decision tree model to identify and diagnose motor speech disorders; they normed their model on children age 6 years and older.

Assessment of impairment should include evaluation of the integrity of structural as well as functional aspects of the speech mechanism, because abnormal resting postures and actions of oropharyngeal muscles can lead to abnormalities in the dental arches, poor control of oral secretions, and an increased risk for middle ear infections. The use of detailed, comprehensive protocols to guide assessment of speech mechanism impairment and interpretation of findings is recommended (e.g., Dworkin and Culatta, 1995; St. Louis and Ruscello, 2000). Instrumental procedures that assess the function of the various speech subsystems (respiratory, laryngeal, velopharyngeal, and oral articulatory) also help to determine the nature and severity of impairment if child cooperation allows (Murdoch, Johnson, and Theodoros, 1997). Procedures for assessing various aspects of speech function (e.g., phonological system and phonetic adequacy, intelligibility, prosody) and speech ability that can be repeated across time to index change are described in Hodge and Wellman (1999) and Yorkston et al. (1999). In addition to perceptual measures, acoustic measures such as second formant onset and extent and vowel area have been shown to be sensitive to both effective and ineffective compensatory articulation strategies used by children with motor speech disorders (e.g., Nelson and Hodge, 2000).

When making decisions about intervention, the clinician also needs to assess the child's feeding behavior, cognitive and receptive and expressive language skills, hearing, psychosocial status and motivation to speak and communicate, gross and fine motor skills, general health and stamina, and the child's family situation, including family members' goals and perspectives. A multidisciplinary team approach to assessment and intervention planning, with ongoing involvement of the family in selecting, coordinating, and evaluating treatment service options, is critical to the successful management of children with motor speech disorders (Mitchell and Mahoney, 1995).

At present, most childhood motor speech disorders are considered to be chronic because they are the result of brain damage or dysgenesis, for which there is no cure. It is expected that the neurological diagnosis associated with the motor speech disorder will be chronic and may affect the child's academic, social, and vocational future. However, appropriate and sufficient treatment can significantly improve these children's communication effectiveness (Hodge and Wellman, 1999; Love, 2000). The overall goal of treatment is to help these children communicate in the most successful and independent manner possible and includes helping them become desirable communication partners. It is unrealistic to expect that these children will be provided with or benefit from continuous treatment from infancy to adulthood. Families have identified the preschool and early school years, and school transitions (i.e., change in schools due to family relocation, elementary to junior high, junior to senior high, and then to college), as times when the knowledge and support of speech-language pathologists is particularly needed. Children with a congenital or early-onset condition that results in a motor speech disorder must learn how to produce the phonological system of their language with reduced control of the muscle groups used to produce and shape the sound contrasts that signal meaning to their listeners. Explicit, goal-directed opportunities for extensive practice in producing and combining speech sounds in meaningful utterances are typically required for these children to attain their potential for learning their phonological system, its phonetic realization, and making their speech intelligible. In addition to speech development, the child's language, cognitive, and social development is also at risk because of the important role that speech plays in development. Children who suffer neurological insult after the primary period of speech development has occurred (e.g., after 3–4 years of age) are faced with the task of relearning a system that has been acquired with normal speech motor control, so they have internal models of their phonological-phonetic system in place. For these children, the focus is on relearning these, and then monitoring and providing support as needed for acquisition of new spoken language skills that had not been acquired at the time of the neurological insult.

Treatment planning for all children with motor speech disorders should include a team approach that promotes active family involvement in making decisions and implementing treatment, attention to principles of motor learning at a level that is developmentally appropriate to the child (Hodge and Wellman, 1999), consideration of a variety of service delivery forms, and a holistic view of the child with a motor speech problem (Mitchell and Mahoney, 1995). Training tasks need to be goal-directed and should actively engage and involve the child as a problem solver. Because learning is context-specific, training activities should simulate real-world tasks as much as possible and be enjoyed by the child. Training goals should build on previously learned skills and behaviors. The child must have multiple opportunities to practice attaining each goal, and should have knowledge of results.

A combination of treatment approaches that address multiple levels of the communication disorder (impairment, speech functional impairment, and ability to communicate in various contexts) is typically used in management programs for children with motor speech disorders. The particular approaches change with the child's and family's needs and as the child's abilities change. Possible approaches include the following (Hodge and Wellman, 1999; Yorkston et al., 1999; Love, 2000):