I. Motor developmental delays/disorders
1. Developmental indicators/milestone delays include simple motor developmental lag, language developmental lag, or cognitive developmental lag.
Motor developmental delays include gross motor and fine motor. Recent studies suggest that the disorder should also include lags in sleep pattern changes. Children should be evaluated when they do not respond to sound or visual stimuli at 6 weeks of age, do not respond socially at 3 months of age, still have poor head control at 6 months of age, do not sit at 9 months of age, do not use their fingers at 12 months of age, do not walk or say single words at 18 months of age, do not run or say words at 2 years of age, and cannot climb stairs or communicate with simple words at 3 years of age. Crawling may be missed because the child does not need to perform it, so it should not be used as an indicator of developmental milestones. Ninety percent of children who are developmentally delayed in one area alone do not require medical intervention and will develop normally in the future. Approximately 10% of children will require medical intervention. Early screening and early intervention are good for prognosis.
2.Comprehensive developmental delay
GDD is diagnosed in children under 5 years of age in early development who are behind in multiple developmental milestones, too young to complete a standardized systematic test of intellectual functioning, and whose severity level cannot be assessed with certainty, but should be reassessed after a period of time. The incidence is about 3%. Common causes include genetic disorders, embryonic drug or toxic teratology, environmental deprivation, intrauterine malnutrition, intrauterine hypoxia, intrauterine infection, trauma, encephalopathy of prematurity, central nervous system trauma and infection during infancy, and lead poisoning.
3.Developmental coordination disorders
(1) The acquisition and execution of motor coordination is lower than the motor skills that should be acquired by normal peers, and movements are clumsy, slow, and imprecise.
(2) This motor disorder can continuously and significantly affect daily life and school, work, and even recreation.
(3) The impairment appears early in development.
(4) The deficit in motor skills cannot be explained by mental retardation or visual impairment; nor is it due to motor impairment caused by cerebral palsy, muscular dystrophy, or degenerative disease.
4. Autism spectrum disorders
(1) Persistent multi-situational deficits in social communication and social interaction that currently exist or have existed.
(2) Restrictive, repetitive behaviors, interests, or activity patterns that are abnormal. At least 2 of the following 4 items are required and may be present or historical: stereotyped or repetitive motor movements, object use, or speech; persistent sameness, inflexibility, or ritualized verbal or nonverbal behavior patterns; highly restricted fixed interests that are abnormal in intensity and concentration; over- or under-responsiveness to sensory input, or unusual interest in perception of the environment Unusual interest in perception of the environment.
(3) Symptoms appear early in development, perhaps early on when they are not evident or are masked by stages of learning due to the constraints of the social environment.
(4) the symptoms result in very severe functional deficits in many socially important areas
(5) The deficits cannot be explained by intellectual disability or GDD, and sometimes when intellectual disability and ASD are combined, social communication skills are often below the level of intellectual disability. Some children with ASD may have motor delays that can be mistaken for GDD or early manifestations of cerebral palsy.
Skeletal disorders
1, developmental congenital hip dislocation is a disease caused by genetics, breech birth, leg binding and other factors that cause unilateral or bilateral hip instability and poor alignment of the femoral head and acetabulum. It can be diagnosed by pelvic X-ray, CT and MRI, and has normal intelligence and upper limb motor function but difficulty in standing.
2, congenital ligamentous laxity, delayed development of gross motor development, delayed walking alone, unstable walking, easy to fall, difficulty in walking up and down stairs, significantly increased range of motion of joints and hyperextension, adduction or abduction, normal muscle strength, normal tendon reflexes, no pathological reflexes, no convulsions, normal intelligence, family history may be present, symptoms gradually improve with age.
C. Crestal medullary disease
If necessary, MRI of the crestal medulla should be done to rule out crestal cavitation, crestal medullary compression and crestal myasthenia gravis.
Endocrine diseases
Congenital hypothyroidism: low response, low cry, low body temperature, slow pulse, low intelligence, low muscle tone and other signs of physiologic hypofunction. It can be differentiated from cerebral palsy by special facial features, reduced serum free thyroxine, increased TSH, and delayed bone age.
V. Autoimmune diseases
Multiple sclerosis is an autoimmune disease characterized by inflammatory demyelinating lesions in the white matter of the central nervous system. The most commonly affected sites are the periventricular white matter, optic nerve, cremaster, brainstem, and cerebellum. The main clinical features are multiple foci in the white matter of the CNS with remitting relapses during the course of the disease, spatial multiplicity of signs and symptoms, and temporal multiplicity of the disease course.
5 early signs of abnormal motor development.
(1) weakness of the body.
(2) Significantly less kicking and stirring movements.
(3) abnormal gait during walking.
(4) Asymmetry of movement on both sides.
(5) Inability to grasp accurately.
VI. Common hereditary disorders
Some hereditary disorders have movement disorders, postural abnormalities and altered muscle tone, which are easily misdiagnosed as cerebral palsy, such as ankylosing muscular dystrophy, Duchenne muscular dystrophy, trisomy 21, infantile progressive myelomeningocele, arginase deficiency, heterozygous cerebral leukodystrophy, adrenal cerebral leukodystrophy, familial (hereditary) spastic paraplegia, dopa-sensitive dystonia, glutaric aciduria type I, acetone dystrophy, and dopamine dystrophy. Glutaric aciduria type I, pyruvate dehydrogenase complex deficiency, Rett syndrome, neuronal waxy lipofuscinosis, familial cerebral leukodystrophy/congenital extracortical axonal aplasia (Permet’s disease), ataxia capillaris.