Congenital conditions (Hydrocephalus (signs and symptoms (bulging fontanel…
The basal ganglia also can be affected, resulting in extrapyramidal or dyskinetic cerebral palsy.
However, the term brain is also susceptible to hypoperfusion, which mostly targets watershed areas of the cortex (eg, end zones of the major cerebral arteries), resulting in spastic quadriplegic cerebral palsy.
At term, when circulation to the brain most resembles adult cerebral circulation, vascular injuries at this time tend to occur most often in the distribution of the middle cerebral artery, resulting in a spastic hemiplegic cerebral palsy.
Because these areas carry fibers responsible for the motor control and muscle tone of the legs, injury can result in spastic diplegia (ie, predominant spasticity and weakness of the legs, with or without arm involvement to a lesser degree).
Between weeks 26 and 34 of gestation, the periventricular white matter areas near the lateral ventricles are most susceptible to injury.
Hypoperfusion can result in germinal matrix hemorrhages or periventricular leukomalacia.
Before term, the distribution of fetal circulation to the brain results in the tendency for hypoperfusion to the periventricular white matter.
Brain injury due to vascular insufficiency depends on various factors at the time of injury, including the vascular distribution to the brain, the efficiency of cerebral blood flow and regulation of blood flow, and the biochemical response of brain tissue to decreased oxygenation.
Injury between the 34th and 40th weeks can result in focal or multifocal cerebral injury.
Injury between the 26th and 34th weeks can result in periventricular leukomalacia (foci of coagulative necrosis in the white matter adjacent to the lateral ventricles).
Cerebral injury before the 20th week of gestation can result in a neuronal migration deficit.
Given the complexity of prenatal and neonatal brain development, injury or abnormal development may occur at any time, resulting in the varied clinical presentations of cerebral palsy (whether due to a genetic abnormality, toxic or infectious etiology, or vascular insufficiency).
Brain damage. It may be caused by damage to the parts of the brain that control movement; this damage generally occurs during the fetal or perinatal period, particularly in premature infants.
Interference with oxygen supply. Any process that interferes with the oxygen supply to the brain, such as separation of the placenta, compression of the cord, or bleeding, may cause cerebral palsy.
Maternal infection. Infection that occurs to the mother during the prenatal period, like cytomegalovirus, toxoplasmosis, or rubella, may lead to cerebral palsy.
Nutritional deficiencies. Nutritional deficiencies that may affect brain growth during prenatal period could cause cerebral palsy.
Kernicterus. Kernicterus is a condition that causes brain damage caused by jaundice resulting from Rh incompatibility.
Teratogenic factors. Teratogenic factors such as drugs and radiation can cause cerebral palsy.
Prematurity. Prematurity because immature blood vessels predispose the neonate to cerebral hemorrhage.
signs and symptoms
bulging fontanel, which is the soft spot on the surface of the skull.
a rapid increase in head circumference.
eyes that are fixed downward.
Premature birth: Infants born preterm have a higher risk of intraventricular hemorrhage, or bleeding within the ventricles of the brain, which may result in hydrocephalus.
Problems during pregnancy: An infection in the uterus during pregnancy increases the risk of hydrocephalus in the developing fetus
Problems with fetal development: Examples include incomplete closure of the spinal column.
a limited attention span
physical coordination problems
problems with memory
A nurse should know how to measure the fluid intake and output
Ensure the full fluid suctioning of the head
follow the good measure of sterility when doing certain procedure
Ensure the good drainage of the cerebrospinal fluid
Assess for the level of sepsis and give antibiotics as prescribed by the doctor
Mornitor vital signs and weigh a patient
Cerebral palsy (CP), defined as a group of nonprogressive disorders of movement and posture, is the most common cause of severe neurodisability in children
Interruption of oxygen supply to the fetus or brain asphyxia was classically considered to be the main causal factor explaining later CP. Ho
ongenital malformations are rarely identified. CP is most often the result of environmental factors, which might interact with genetic vulnerabilities, and could be severe enough to cause the destructive injuries visible with standard imaging (i.e., ultrasonographic study or MRI), predominantly in the white matter in preterm infants and in the gray matter and the brainstem nuclei in full-term newborns
Moreover they act on an immature brain and could alter the remarkable series of developmental events. Biochemical key factors originating in cell death or cell process loss, observed in hypoxic-ischemic as well as inflammatory conditions, are excessive production of proinflammatory cytokines, oxidative stress, maternal growth factor deprivation, extracellular matrix modifications, and excessive release of glutamate, triggering the excitotoxic cascade.
Only two strategies have succeeded in decreasing CP in 2-year-old children: hypothermia in full-term newborns with moderate neonatal encephalopathy and administration of magnesium sulfate to mothers in preterm labor.
Medical conditions of the mother―Mothers with thyroid problems, intellectual disability, or seizures have a slightly higher risk of having a child with CP.
Birth complications―Detachment of the placenta, uterine rupture, or problems with the umbilical cord during birth can disrupt oxygen supply to the baby and result in CP.
Infections during pregnancy―Infections can lead to increases in certain proteins called cytokines that circulate in the brain and blood of the baby during pregnancy.
Low birthweight―Children who weigh less than 5 1/2 pounds (2,500 grams) at birth, and especially those who weigh less than 3 pounds, 5 ounces (1,500 grams)
Signs and symptoms
Muscular: difficulty walking, difficulty with bodily movements, muscle rigidity,
permanent shortening of muscle, problems with coordination, stiff muscles, overactive reflexes,
involuntary movements, muscle weakness, muscle spasms, or paralysis of one side of the body
Developmental: failure to thrive, learning disability, slow growth, or speech delay in a child
Speech: speech disorder or stuttering
Also common: constipation,
difficulty raising the foot, difficulty swallowing, drooling, hearing loss, leaking of urine, paralysis,
physical deformity, scissor gait, seizures, spastic gait, teeth grinding, or tremor