About Cerebal Palsy

What causes Cerebral Palsy?

Cerebral palsy is the result of damage to the baby’s developing brain before, during, or shortly after birth.

Infection of the mother during pregnancy, neonatal jaundice (kernicterus), lack of oxygen supply (hypoxia/anoxia), brain hemorrhage, and abnormal brain development can all contribute to the onset of cerebral palsy in a child. The following are some causes of cerebral palsy:

Oxygen Deprevation

Cerebral palsy may develop if the brain of a fetus or newborn is deprived of oxygen, rendering it unresponsive and possibly causing neurological damage. Brain oxygen deprivation can be divided into two categories: hypoxia, in which oxygen levels are diminished, and anoxia, in which oxygen levels are eliminated entirely. In contrast to anoxia, which is believed to be a more severe cause of CP symptoms, hypoxia is frequently blamed for the mild manifestations of the disorder.

Umbilical cord severing, umbilical cord pinching, and a prolapsed umbilical cord are just a few of the many potential causes of anoxia and hypoxia. In addition, infants who are born prematurely and who require prolonged intubation are at an increased risk of suffering from oxygen deprivation, which can ultimately result in cerebral palsy.

How does oxygen deprivation contribute to CP?

In each and every cell that makes up the human body, oxygen is indispensable for the continuation of life. When brain cells receive an insufficient or nonexistent oxygen supply, the cells’ ability to survive and thrive in the brain is compromised. A lack of oxygen in the brain causes cell death and interferes with the normal transmission of signals to the muscles they regulate. Directly resulting from this is brain damage, which in turn leads to cerebral palsy.

Brain Bleed

Cerebral hemorrhage, or simply “brain bleeding,” occurs when a blood vessel in the brain bursts and blood leaks into the brain. Intraventricular hemorrhage (IVH) and other neurological complications can develop if this condition is left untreated, as it causes fluid to accumulate in the ventricles of the brain. IVH can result in permanent injury and is graded from I to IV as follows:

Grade I: Isolation of the bleeding within the germinal matrix (GMH).
Grade II: Germinal Matrix Hemorrhage (GMH) accompanied by intraventricular hemorrhage (IVH) without ventricular enlargement
Grade III: GMH and IVH along with ventricular enlargement.
Grade IV: GMH and IVH along with intraparenchymal hemorrhage

A common but potentially fatal complication of preterm birth is the presence of a hematoma in the newborn’s brain. The incidence is highest before 28 weeks of pregnancy. A hematoma is a collection of blood in the brain caused by a fracture of the skull or a tear in the membranes separating the skull from the brain. In a premature infant, a hematoma like this has the potential to cause or contribute to permanent brain damage.

Although early screening and intervention have reduced the incidence of cerebral palsy in the United States, the incidence of brain injury among premature infants continues to rise. The most influential factors in determining whether or not a child will sustain a brain injury are those associated with premature births, such as an advanced gestational age and a greater birth weight. Cerebral palsy occurs in about 15% of extremely low-birth-weight infants and 20% of very low-birth-weight infants.

With such a low total blood volume, the newborn baby’s blood vessels are able to pump blood to the brain incredibly quickly. The brain’s blood vessels are especially vulnerable because their thin walls allow for easy rupture.

Hydrocephalus

Formerly known as “water on the brain,” the condition known today as hydrocephalus more accurately refers to the accumulation of cerebrospinal fluid (CSF) within the skull as opposed to the presence of water. The cerebrospinal fluid (CSF) is the fluid that surrounds and fills the brain and spinal cord. It acts as a cushion for the brain, maintains constant intracranial pressure, and removes potentially harmful substances from the brain. When cerebrospinal fluid (CSF) cannot flow freely, it will begin to accumulate within the skull, putting pressure on the tissues of the brain. If left untreated, this prolonged accumulation of fluid and elevated pressure can either cause direct damage to brain tissues or prevent the brain from receiving an adequate supply of oxygen and blood, ultimately leading to cerebral palsy.

Numerous factors, including malformations or genetic conditions, hemorrhage, infections such as meningitis, trauma sustained during delivery or after birth, tumors and cysts, etc., can result in hydrocephalus.

The treatment for severe hydrocephalus is the installation of a shunt that acts as a drainage system for the CSF, allowing it to flow away from the brain and decreasing the pressure around it to prevent damage. The shunt consists of a tube with an attached valve that opens at a predetermined pressure level and closes when the pressure returns to normal.

Jaundice and Kernicterus

About 60% of all newborns suffer from jaundice, which causes their skin to turn yellow. Jaundice is caused by the accumulation of bilirubin in a baby’s blood. As bilirubin levels increase, jaundice typically spreads from the face to the chest, abdomen, arms, and legs. Additionally, the whites of the eyes can appear yellow. Babies with darker skin will have their gums and inner lips examined for jaundice.

Although the mother’s liver is responsible for clearing bilirubin from the baby’s system during pregnancy, the newborn’s liver is responsible for doing so after birth. Some newborns’ livers may not be fully developed, preventing them from effectively eliminating bilirubin. This is particularly true for infants born prematurely before 37 weeks of pregnancy.

Particularly susceptible to developing jaundice are newborns with Mediterranean or East Asian ancestry, babies who eat poorly in their first few days of life, babies born with bruises, and babies whose mothers have a negative RH blood type.

If severe jaundice is allowed to persist untreated for an extended period of time, the condition known as kernicterus may eventually manifest. Kernicterus is a form of brain damage that can be caused by high levels of bilirubin (bilirubin toxicity) in a newborn’s blood. This disorder has been associated with dyskinetic cerebral palsy (such as athetoid cerebral palsy and dystonic cerebral palsy). In addition to cerebral palsy kernicterus can also cause hearing, vision and dental problems, and can sometimes lead to mental retardation. To decrease the risk of developing kernicterus, jaundice should be diagnosed and treated without delay.

If your baby has yellow or orange skin, is difficult to wake up or won’t sleep, isn’t breast feeding or sucking on a bottle well, is very fussy/grumpy, or doesn’t have enough wet or dirty diapers (at least 4-6 thoroughly wet diapers in 24 hours and 3 to 4 stools per day by the fourth day), you should schedule an appointment with your doctor right away. If your child is crying inconsolably or at a very high pitch, is arched like a bow (the head or neck and heels are bent backwards while the body is bent forward), has a stiff, limp, or floppy body, or has unusual eye movements, you should immediately take him or her to the emergency department of your nearest hospital.

Your baby’s diet should not be neglected while he or she is being treated for jaundice. Your baby’s bilirubin levels will naturally decrease as he or she begins to eliminate waste more frequently through urination and defecation as a result of a proper diet. Providing your baby with plenty of breast milk on a regular basis will aid in reducing his or her bilirubin levels. Do not hesitate to consult your medical practitioner if you are experiencing difficulties while breastfeeding.

Screening for jaundice in newborns should occur every 8 to 12 hours for the first 48 hours after birth, and then on a consistent basis between the ages of 3 and 5 days, which is typically when bilirubin levels are at their highest. If your newborn is discharged from the hospital earlier than 72 hours after birth, it is advised that you bring him or her to the pediatrician within the first 48 hours of being at home to ensure there are no signs of jaundice. Your child’s age at the time of hospital discharge and other factors will determine the best time for this visit.

Your local physician may perform a bilirubin level test on your infant by placing a light meter on the infant’s head. As a result, a level of transcutaneous bilirubin (TcB) is produced, and if it is elevated, a blood test from the baby’s heel is likely to be ordered, resulting in a total serum bilirubin (TSB) level. If the level is still high, treatment will most likely be administered after taking into account the baby’s age in hours as well as other risk factors. In the event that treatment is administered, it is likely that additional blood samples will be taken to monitor the level of TSB and ensure that it is decreasing as the physician intended. Treatment options include phototherapy, in which the infant is exposed to a light that breaks down bilirubin into a form that can be flushed out of the body via urine and feces. If your child’s bilirubin levels are too high to be treated effectively by phototherapy alone, a blood transfusion may be required in order to prevent neurological damage from occurring.

If your baby has been diagnosed with jaundice, it is critical that you take the condition seriously and adhere to all of the recommended appointments and medical care. (https://www.cdc.gov/ncbddd/jaundice/facts.html)

Types of Cerebral Palsy

Cerebral palsy can be divided into multiple main categories and subcategories based on the affected brain region and the patient’s symptoms. For instance, spastic cerebral palsy causes abnormally high muscle tone in multiple limbs or throughout the entire body, dyskinetic cerebral palsy causes uncontrolled movements throughout the entirety of the body, and ataxic cerebral palsy affects a person’s balance and coordination. Some individuals may develop a combination of these various types of cerebral palsy, which is commonly referred to as mixed cerebral palsy.

Spastic Cerebral Palsy

The majority of individuals with cerebral palsy have a type known as spastic cerebral palsy. Spastic cerebral palsy causes children to have stiff and sometimes painful muscles, as well as overly exaggerated reflexes (spasticity). The majority of affected individuals will have trouble walking, though the degree of difficulty will vary depending on the severity of the spasticity. Affected individuals may also experience difficulties with fine motor skills, and actions such as closing buttons or holding a pen may be particularly challenging.

There are three distinct types of spastic cerebral palsy, defined by the body regions they primarily affect. Spastic diplegia primarily affects a person’s arms, in contrast to spastic hemiplegia, which affects only one side of the body, and spastic quadriplegia, which affects the entire body up to the neck.

Spastic Diplegia

Children with spastic diplegia, also known as diplegic cerebral palsy, may exhibit a variety of symptoms and characteristics. Due to tightness in the hips and legs, they may walk with a scissor gait; if spasticity in the calves is particularly severe, they may walk on their toes and have difficulty maintaining their balance.

Diplegic cerebral palsy is frequently diagnosed in infancy, before the baby has reached typical developmental milestones.

Crawling with the arms rather than the legs or not crawling at all is a major red flag for medical professionals who are attempting to diagnose this form of cerebral palsy in infants or toddlers.

Spastic Hemiplegia

Spastic hemiplegia is a form of cerebral palsy that affects only one side of the body, most notably the arm, while the corresponding leg retains some function.

A child typically develops spastic hemiplegic cerebral palsy within the first year of life. There is a noticeable delay in physical development and a lack of age-appropriate skills (sitting, crawling, and walking). Children with spastic hemiplegia stand on their affected leg’s toes and shift their body weight to their healthy leg to compensate. Over time, spastic hemiplegic cerebral palsy worsens the growth retardation of affected limbs and further impairs balance. Most children with spastic hemiplegia will eventually learn to walk, despite their asymmetrical growth, but the most severe cases will require the use of a wheelchair.

Fine motor skills such as writing and button opening and closing may be especially challenging. The affected side of the body is characterized by pronounced muscle stiffness and weakness. When the affected side of the body is neglected and underutilized during daily activities, it can result in poor bilateral coordination and make it significantly more challenging to perform daily tasks.

Spastic Quadriplegia

As the most severe form of spastic cerebral palsy, spastic quadriplegia limits a person’s mobility significantly. It manifests as impaired muscle control and coordination across the four limbs, trunk and face. Mouth muscles may be affected, interfering with normal functions such as speaking, chewing, and swallowing. Typically, individuals with spastic quadriplegia have motor impairments in the upper body that are comparable to or worse than those in the lower body.

Although the severity of spastic quadriplegia varies from child to child, all children with this condition face a lifetime of physical and emotional challenges. Children with mild forms of the disease may eventually be able to sit and walk independently for short distances, whereas those with severe forms of the disease struggle to perform even the most basic of tasks.

Because spastic quadriplegic cerebral palsy results in a severe lack of physical activity, poor posture, and low muscle mass, additional complications may arise as the affected child ages, including musculoskeletal deformities (such as scoliosis and ankle equinus, among others), joint subluxation or dislocation, poor quality sleep, chronic pain, pressure sores, and osteoporosis.

Dyskinetic Cerebral Palsy

Following spastic forms, dyskinetic cerebral palsy (DCP), also called athetoid cerebral palsy, is the second most common form of the disorder. It is characterized by abnormal regulation of muscle tone, resulting in undesirable fluctuations between hypotonia (low muscle tone) and hypertonia (high muscle tone) and affecting primarily the arms, hands, and legs. The daily variations in tone result in uncontrolled movements that can make it difficult to regulate and coordinate the growth and fine motor functions of the entire body. Dyskinetic cerebral palsy is caused by damage to very specific regions of the brain, specifically the basal ganglia and/or thalamus.

Individuals suffering from dyskinetic cerebral palsy experience slow, writhing movements interspersed with periods of rapid, jerky movement. More specifically, dyskinetic/athetoid cerebral palsy encompasses three distinct movement disorders:

Athetosis is characterized by movements that are extremely erratic, slow, involuntary, tangled, and writhing.

Dystonia is characterized by the involuntary contraction of muscles. This involuntary muscle contraction can manifest in a variety of different ways, such as a twitch or a movement that repeats itself.

Chorea causes the affected person to make rapid, jerky movements that are neither rhythmic nor repetitive but instead appear to progress from one muscle to the next. Chorea happens without the will of an individual to make a movement. Chorea, and athetosis often coexists and together create more complex, contorted motions.

Problems with fine and gross motor skills, such as grasping, sitting, and walking, are symptoms of all three of the aforementioned movement disorders, which can coexist in a variety of combinations.

Dyskinetic cerebral palsy is especially challenging because of the severity of its motor impairments and the involuntary movements that are characteristic of the disorder. Patients with dyskinetic CP often have a hard time maintaining a healthy weight due to eating difficulties caused by dysphagia and the increased energy expenditure caused by their involuntary movements.

In addition to motor impairment, more than half of individuals with DCP may experience non-motor complications such as pain and musculoskeletal deformities, language and communication difficulties, epilepsy, difficulty seeing and hearing, etc.

Ataxic Cerebral Palsy

Ataxic cerebral palsy is the rarest form of the condition. It is characterized by difficulties with both balance and coordination as a result of damage to the cerebellum, a brain region responsible for these functions. Those with ataxic cerebral palsy have difficulty maintaining balance while standing or walking, have poor coordination that makes even writing difficult, have generally shaky movements (including nystagmus of the eyes), and tire easily when performing physically demanding tasks. Speech may sound slower than normal and lack rhythm. Muscle hypotonia (weakness) is often the earliest sign of ataxic cerebral palsy, which typically appears between six months and one year. Atypically flaccid limbs are common in children of this age and may prevent them from reaching developmental milestones on time.