DSM-IV-TR Diagnostic Criteria
Performance in daily activities that require motor coordination is substantially below that expected given the person's chronological age and measured intelligence. This may be manifested by marked delays in achieving motor milestones (e.g., walking, crawling, sitting), dropping things, “clumsiness,” poor performance in sports, or poor handwriting.
The disturbance in Criterion A significantly interferes with academic achievement or activities of daily living.
The disturbance is not due to a general medical condition (e.g., cerebral palsy, hemiplegia, or muscular dystrophy) and does not meet criteria for a pervasive developmental disorder.
If mental retardation is present, the motor difficulties are in excess of those usually associated with it.
(Reprinted, with permission, from Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Text Revision Copyright 2000 American Psychiatric Association.)
Recent research suggests that developmental coordination disorder can be divided into several subcategories (Table 33–1).
Table 33–1. Subcategories of Developmental Coordination Disorder |Favorite Table|Download (.pdf)
Table 33–1. Subcategories of Developmental Coordination Disorder
Clumsiness: inefficiency in the performance of fine motor movements
Adventitious movements: synkinesis, chorea, tremor, or tics
Dyspraxia: inability to learn or perform serial voluntary movements to complete skilled acts
Material-specific dyspraxia: motor execution below expected for age with regard to writing (dysgraphia), drawing (constructional dyspraxia), or speech (verbal dyspraxia)
Neurologic soft signs: nonnormative performance on motor or sensory neurologic tests in the absence of localizable neurologic disease or defect
Pathologic handedness: left-handedness associated with left-hemispheric defect and paresis of the right hand
It is estimated that 6% of schoolchildren have developmental coordination disorder. Children with perceptual motor defects have a high incidence of educational problems and psychological maladjustment.
Motor development involves the gradual acquisition of central control over reflex movement. There is controversy over whether this acquisition involves the suppression of reflex and spontaneous cyclic movements of early infancy or whether infantile movements are incorporated into the elements that become voluntary motor skills.
Skilled movement requires a program of action with a specified objective or set goal. The program is composed of a sequence of hierarchically organized subroutines under executive control. Once acquired, motor skills are flexible. For example, the child who has learned to walk can do so on smooth, rugged, soft, or hard surfaces. The adaptation to different situations of the programmed subroutines requires accurate perception, central processing, executive control, and progressive feedback. Feedback monitors the approximation of the program to the set goal and modifies the timing, speed, force, and direction of movement until the desired endpoint is achieved. Initially, feedback produces jerky movements, as the child struggles to master the skill. Eventually, the skill is regulated centrally and the subroutines automated. A variety of skills can be built up from a limited number of practiced subroutines deployed in accordance with combinatorial rules. The combinatorial rules act as a kind of grammar, organizing the subroutines in hierarchical fashion. Skilled performance can be delayed or disrupted if basic reflexes are not suppressed or incorporated into the program, or if the following functions are delayed, defective, or disrupted: Perception, central processing and programming, motor function, or feedback.
The hypothesis of minimal brain damage or minimal brain dysfunction was formerly invoked to explain minor sensorimotor abnormalities or immaturities, however, there is no way to prove this hypothesis. It is unclear whether the defects or delays occur in the peripheral or in the central apparatus or, if so, how they relate to developmental coordination disorder.
Like many other neurodevelopmental disorders of childhood onset, it is likely that there are multiple vulnerability genes associated with this condition. None, however, have been identified as yet.
The clumsy child is slow, jerky, and inefficient in fine-motor performance. Agonist and antagonist muscles are poorly coordinated. Motor milestones are delayed. The child drops things, tends to lose his or her balance, and is poor at activities requiring hand-eye coordination. Clumsiness can affect a particular set of muscles (e.g., orofacial, hand and finger, shoulder girdle), several sets, or the entire body musculature. The child's social development is likely to be affected, particularly if clumsiness is associated with learning problems.
These movements involve one or more of the following unwilled movements during a purposeful motor activity: synkinesis, chorea, tremor, or tic.
Synkinesis refers to movement in a set of muscles other than that in which the primary motor action takes place. It may be homologous (i.e., symmetrical) or heterologous (i.e., asymmetrical). For example, while drawing with the right hand, the child with synkinesis moves his or her left hand (homologous) or tongue (heterologous). Chorea refers to repetitive abrupt movements of the limbs or face. Tremor refers to rhythmic oscillations of a body part. A tic is an abrupt, involuntary, repetitive movement of a particular set of muscles, usually in the face, mouth, head, neck, or diaphragm.
Despite normal strength, coordination, and perception, the dyspraxic child is unable to learn or perform motor skills. Dyspraxia may involve all effector muscles or may affect mainly the orofacial musculature, hand, or trunk and lower limb. The components of the motor skill are intact, but they are combined in an incoherent manner. A clumsy child will slowly get the job done. The dyspraxic child will not get the job done at all.
Children with material-specific dyspraxia exhibit defective motor performance in regard to specific tasks such as handwriting (specific dysgraphia), drawing and construction (constructional dyspraxia), or the articulation of words (verbal dyspraxia).
Found normally in younger children, neurologic soft signs represent a heterogeneous group of phenomena that disappear with normal development. Soft signs are regarded as abnormal if detected beyond a normative cut-off age (8–10 years). They are usually found incidentally unless tested for specifically. Their reliability, validity, and significance are disputed. A number of studies have suggested an association with cognitive dysfunction, learning problems, and psychiatric disturbance. In some cases soft signs may be related to mild brain damage; in other cases they may be related to a genetically determined factor that also correlates with a nonspecific vulnerability to psychiatric disturbance.
Pathologic left-handedness occurs following damage during early development to the left hemisphere, causing a shift from right- to left-handedness. Right-sided hypoplasia, impaired visuospatial functioning, and language impairment are often found in association with this condition.
After taking a developmental history, processing questions directed at elucidating motor performance, and administering a neurologic examination, the clinician can apply the specific assessment procedures described in the following sections:
Gubbay's standardized test battery for the assessment of clumsy children, Denckla's Finger Tapping Test, and Rapin et al.'s Peg-Moving Procedures Test for Clumsiness are useful screening instruments.
The Fog Test and Wolff et al.'s procedure screen for synkinesis are useful. In order to elicit choreiform movements, Wolff and Hurwitz had children stand with their eyes closed; arm, wrists, and fingers extended; and wrists pronated.
The Lincoln-Oseretsky Test includes a subtest for dyspraxia. Dyspraxia can be tested by having the child imitate hand postures, pantomime manual activities, and use actual objects (e.g., pen, cup) in an appropriate way.
Dysgraphia is tested by observing handwriting. Constructional dyspraxia is tested by having the child copy drawings (e.g., the Bender-Gestalt Test) or block designs. Verbal dyspraxia is screened for using the Reynell Developmental Language Scales.
Neurologic soft signs can be screened for with the Physical and Neurological Examination for Soft Signs or the Examination for Minor Neurological Signs in Children. The Examination for Minor Neurological Signs tests the following: Digit span, visual tracking, speech, nystagmus, eye symmetry, hand dominance, crossed dominance of arm and leg, right-left self-identification, right-left identification on examiner, bilateral hand stimulation, face-hand apposition, finger localization, graphesthesia, stereognosis, synkinesis, finger-to-nose apposition, diadochokinesis, and passive head turning.
Additional psychological testing should be undertaken if there is evidence of attentional difficulties or specific areas learning disability.
Laboratory tests are seldom necessary in the evaluation of clumsiness unless there are abnormal findings on neurologic examination or a history of acute changes in motor skills. However, measurement of creatine kinase and lactate dehydrogenase should be performed with children who have reduced muscle mass or limited capacity for physical exertion.
Abnormal findings on neurological examination suggestive of a focal brain abnormality should have magnetic resonance imaging studies or computed tomography as part of their evaluation.
Typically, mild and moderate degrees of clumsiness in early childhood improve over development. More severe clumsiness has a less favorable outcome only in regard to motor proficiencies.
Pincus JH: Neurological meaning of soft signs. In: Lewis M (ed). Child and Adolescent Psychiatry: A Comprehensive Textbook, 3rd edn. Philadelphia: Lippincott Williams & Wilkins, 2002, pp. 573–581.
Shafer SO, et al.: Hard thoughts on neurological “soft signs.” In: Rutter M (ed). Developmental Neuropsychiatry. New York: Guilford Press, 1983, pp. 113–143.
Shaffer D, et al.: Neurological “soft signs”: Their origins and significance for behavior. In: Rutter M (ed). Developmental Neuropsychiatry. New York: Guilford Press, 1983, pp. 144–163.
Wilson PH: Practitioner review: Approaches to assessment and treatment of children with DCD: An evaluative review. J Child Psychol Psychiatry
Clumsiness is observed in chronic intoxication with neuroleptic and anticonvulsant drugs, in neuromuscular disorders (e.g., Charcot-Marie-Tooth disease, Duchenne's disease), and in upper motor neuron disorders (e.g., cerebral palsy, degenerative disorders). Children with Down syndrome, autism, Asperger's syndrome, specific dyslexia, and ADHD are sometimes more clumsy than is appropriate for their mental age.
Synkinesis is associated with agenesis of the corpus callosum, Klippel-Feil syndrome, hypogonadism, midline facial defects, and a rare familial syndrome. It may be associated with ADHD and conduct disorder. Chorea is observed in Sydenham's chorea (anti-streptolysin titer and electrocardiogram should be ordered to test for rheumatic fever), hyperthyroidism, benign familial chorea, CNS degenerations (e.g., Wilson's disease, Hallervorden-Spatz disease, homocystinuria, Huntington's disease), and tardive dyskinesia. Tremor is associated with posterior fossa tumors; neuroleptic, lithium, or phenytoin toxicity; hyperthyroidism; and benign familial tremor. Simple motor tics should be distinguished from Tourette's syndrome.
Dyspraxia is associated with subacute sclerosing panencephalitis, HIV encephalopathy, Rett's disorder, and degenerative disorders of the CNS, whether inborn or acquired. Dyspraxia can be associated with learning disorders and possibly ADHD and autism. Dysgraphia and oral-motor dyspraxia may be associated with neurofibromatosis, congenital heart disease, and homocystinuria. Constructional dyspraxia is observed in William's disease. Verbal dyspraxia has been described in galactosemia and fragile-X syndrome.
A number of treatment methods have been proposed, but it is not clear whether any of them is effective. Ayres designed a motor training program based on the theory that motor skills disorders are caused by a failure to inhibit primitive reflexes. Kephart's motor training targets posture, balance, locomotion, manipulation, catching, and propulsion. Bobath and Connolly have designed physiotherapy and occupational therapy techniques for the remediation of motor handicaps.
Complications/Adverse Outcomes of Treatment
All children with developmental difficulties in motor coordination should receive supportive care failure to do so may lead to with increased academic, emotional, and behavioral problems.
Children with motor deficits that continue into adolescence and adulthood are more likely than their peers to have poor social competence, reduced academic motivation, lower self-esteem, obesity, and poorer physical fitness in part due to their reluctance to engage in physical activity and sports.
Connolly K: Motor development and motor disability. In: Rutter M (ed). Developmental Psychiatry. Baltimore: University Park, 1981, pp. 138–153.
Deuel RK: Motor skills disorders. In: Hooper SR, Hynd GW, Mattision RE (eds). Developmental Disorders: Diagnostic Criteria and Clinical Assessment. Hillsdale, NJ: Lawrence Erlbaum Associates, 1992, pp. 239–281.
Gillberg C: Deficits in attention, motor control, and perception: A brief review. Arch Dis Child
Voeller KKS: Nonverbal learning disabilities and motor skills disorders. In: Coffey CE, Brumback RA (eds). Textbook of Pediatric Neuropsychiatry. Washington, DC: American Psychiatric Press, 1998, pp. 719–768.