Cerebral palsy – Wikipedia, the free encyclopedia

Cerebral palsy (CP) is an umbrella term denoting a group of non-progressive,[1][2] non-contagious motor conditions that cause physical disability in human development, chiefly in the various areas of body movement.[3]Scientific consensus still holds that CP is neither genetic nor a disease, and it is also understood that the vast majority of cases are congenital, coming at or about the time of birth, and/or are diagnosed at a very young age rather than during adolescence or adulthood. It can be defined as a central motor dysfunction affecting muscle tone, posture and movement resulting from a permanent, non-progressive defect or lesion of the immature brain.

Cerebral refers to the cerebrum, which is the affected area of the brain. The disorder may often involve connections between the cortex and other parts of the brain such as the cerebellum. The term palsy in modern parlance refers to disorder of movement, but the word root "palsy" does still technically mean "paralysis" today, even though it is not used as such within the meaning of cerebral palsy. The use of "palsy" in the term cerebral palsy makes it important to note that paralytic disorders are in fact not cerebral palsy meaning that the condition of quadriplegia, which comes from spinal cord injury or traumatic brain injury, should not be confused with spastic quadriplegia, which doesn't; nor should tardive dyskinesia be confused with dyskinetic cerebral palsy or the condition of (paralytic) "diplegia" with spastic diplegia. In fact, as of the early 21st century some clinicians have become so distressed at common incorrect use of these terms that they have resorted to new naming schemes rather than trying to reclaim the classic ones; one such example of this evolution is the increasing use of the term bilateral spasticity to refer to spastic diplegia. Such clinicians even argue quite often that the "new" term is technically more clinically accurate than the established term.[citation needed]

Cerebral palsy is caused by damage to the motor control centres of the developing brain and can occur during pregnancy, during childbirth, or after birth up to about age three.[4][5] Resulting limits in movement and posture cause activity limitation and are often accompanied by disturbances of sensation, depth perception, and other sight-based perceptual problems and communication ability; impairments can also be found in cognition, and epilepsy is found in about one-third of cases. CP, no matter what the type, is often accompanied by secondary musculoskeletal problems that arise as a result of the underlying disorder.[6] Cerebral palsy's nature as a broad category means it is defined mostly via several different subtypes, especially the type featuring spasticity, and also mixtures of those subtypes.

Improvements in the care of newborns has helped reduce the number of babies who develop cerebral palsy and increased the survival those with very low birth weights.[7][8] There is no known cure, with medical interventions attempting to treat and prevent complications. In 2009 the rate of CP was 2.24.4 per 1,000 live births in the western world,[9] indicating a slight rise in recent years.

All types of cerebral palsy are characterized by abnormal muscle tone (e.g., slouching over while sitting), reflexes, or motor development and coordination. There can be joint and bone deformities and contractures (permanently fixed, tight muscles and joints). The classical symptoms are spasticities, spasms, other involuntary movements (e.g., facial gestures), unsteady gait, problems with balance, and/or soft tissue findings consisting largely of decreased muscle mass. Scissor walking (where the knees come in and cross) and toe walking (which can contribute to a gait reminiscent of a marionette) are common among people with CP who are able to walk, but taken on the whole, CP symptomatology is very diverse. The effects of cerebral palsy fall on a continuum of motor dysfunction, which may range from slight clumsiness at the mild end of the spectrum to impairments so severe that they render coordinated movement virtually impossible at the other end of the spectrum.

Babies born with severe CP often have an irregular posture; their bodies may be either very floppy or very stiff. Birth defects, such as spinal curvature, a small jawbone, or a small head sometimes occur along with CP. Symptoms may appear or change as a child gets older. Some babies born with CP do not show obvious signs right away. Classically, CP becomes evident when the baby reaches the developmental stage at 612 to 9 months and is starting to mobilise, where preferential use of limbs, asymmetry, or gross motor developmental delay is seen.

Secondary conditions can include seizures, epilepsy, apraxia, dysarthria or other communication disorders, eating problems, sensory impairments, mental retardation, learning disabilities, urinary incontinence, fecal incontinence, and/or behavioural disorders.

Speech and language disorders are common in people with cerebral palsy. The incidence of dysarthria is estimated to range from 31% to 88%.[10] Speech problems are associated with poor respiratory control, laryngeal and velopharyngeal dysfunction, and oral articulation disorders that are due to restricted movement in the oral-facial muscles. There are three major types of dysarthria in cerebral palsy: spastic, dyskinetic (athetosis), and ataxic.

Speech impairments in spastic dysarthria involve four major abnormalities of voluntary movement: spasticity, weakness, limited range of motion, and slowness of movement. Speech mechanism impairment in athetosis involves a disorder in the regulation of breathing patterns, laryngeal dysfunction (monopitch, low, weak, and breathy voice quality). It is also associated with articulatory dysfunction (large range of jaw movements), inappropriate positioning of the tongue, and instability of velar elevation. Athetoid dysarthria is caused by disruption of the internal sensorimotor feedback system for appropriate motor commands, which leads to the generation of faulty movements that are perceived by others as involuntary. Ataxic dysarthria is uncommon in cerebral palsy. The speech characteristics are imprecise consonants, irregular articulatory breakdown, distorted vowels, excess and equal stress, prolonged phonemes, slow rate, monopitch, monoloudness, and harsh voice.[11] Overall language delay is associated with problems of mental retardation, hearing impairment, and learned helplessness.[3] Children with cerebral palsy are at risk of learned helplessness and becoming passive communicators, initiating little communication.[3] Early intervention with this clientele, and their parents, often targets situations in which children communicate with others so that they learn that they can control people and objects in their environment through this communication, including making choices, decisions, and mistakes.[3]

In order for bones to attain their normal shape and size, they require the stresses from normal musculature. Osseous findings will therefore mirror the specific muscular deficits in a given person with CP. The shafts of the bones are often thin (gracile) and become thinner during growth. When compared to these thin shafts (diaphyses), the centres (metaphyses) often appear quite enlarged (ballooning). With lack of use, articular cartilage may atrophy, leading to narrowed joint spaces. Depending on the degree of spasticity, a person with CP may exhibit a variety of angular joint deformities. Because vertebral bodies need vertical gravitational loading forces to develop properly, spasticity and an abnormal gait can hinder proper and/or full bone and skeletal development. People with CP tend to be shorter in height than the average person because their bones are not allowed to grow to their full potential. Sometimes bones grow to different lengths, so the person may have one leg longer than the other.

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Cerebral palsy - Wikipedia, the free encyclopedia