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CEREBRAL PALSY
There are so many definition of cerebral palsy; there are three recurrent
elements that provide the basis for a concise definition.
Regardless of the specific cause, or etiology all people with the cerebral
palsy have a significant problem with controlling movement and posture.
The brain grows most rapidly and develops most profoundly during the
prenatal period and continues to grow rapidly during the early postnatal
years. Insult prior to 3 years of age results in neurological impairments and
motor outcomes - such as Cerebral Palsy - that are characteristic of injury
to the immature brain. An arbitrary upper age limit of 5 or 6 years has been
suggested for assigning the diagnosis of CEREBRAL PALSY.
Distribution Description
Arm and leg on same side involved, arm usually more than
Hemiplegia
leg.
Double Both sides of body involved, but one side more than other,
Hemiplegia arms usually more affected.
• the upper limb is held with the arm adducted and internally rotated,
• the forearm flexed and pronated,
• the wrists flexed,
• and the fingers flexed
• with the thumb pressed into the palm.
Unless, practiced very adequately from an early age, the spasm in the calf
muscles may lead to permanent contractures.
Because of poor dorsiflexion, the child tends to walk with his heel raised on
the affected side and to compensate, abducts the hip and swings the lower
limb or hyper extends the knee.
Dorsiflexion of the foot is easier to perform with the knee flexed. In severe
cases, there is spasm in the trunk muscles of the affected side. This causes
a scoliosis and by raising the pelvis produces an apparent shortening of the
lower limb, which in turn causes further plantar flexion.
The lower part of the face and tongue may be affected and there may be
an internal strabismus on the affected side.
When the child makes a movement with his non - affected limb, the
affected side partially or completely assumes the typical hemiplegic
position.
About two-thirds of the cases of hemiplegia date from birth and about one-
third follow an illness catastrophe in infancy.
1. CONGENITAL
2. ACQUIRED
1. CONGENITAL
a. SW Syndrome:
The condition has a naevus on one side of the face and evidence of a
naevoid condition in the brain, causing a hemiplegia of the opposite side.
There is usually intra-cranial calcification. Mostly these children suffer from
epilepsy and mental retardation.
c. Birth Abnormalities
d. No Apparent Cause
In about 20% of cases, no cause can be found for the condition. There may
have been unsuspected cerebral involvement during birth or a cerebro-
vascular incident.
3. ACQUIRED
During the last few years, we have seen a large number of cases with
acquired hemiplegia. There are numerous causes for the development of
hemiplegia during early life in a previously healthy child.
Growth: The affected limbs may be thinner and shorter than those on the
normal side. This may not be due to lack of use or spasticity but appears to
be cerebral in origin. Shorting of the leg may further increase planter
flexion.
Speech: The motor control of speech is usually normal in hemiplegia unless
there is bilateral involvement of the face and muscles used for speech. This
occurs in occasional case of congenital suprabulbar palsy. Hemiplegic
children may have delayed language development due to mental
retardation; but there may be specific dysphasia due to damage to the
speech centers in the affected hemisphere.
Epilepsy: Epileptic attacks occur very commonly. The fits may date from
birth or occur for the first time in infancy, childhood or adolescence. There
may be frequent fits or an occasional episode. Onset of epilepsy before
three years appears to have a poor prognosis for later intelligence.
The placement of adult hemiplegic possibly with more organized early help
the results could be better. The majority of hemiplegics with / without
supervision can work in open market.
CEREBRAL PALSY SPASTIC DIPLEGIA
This is the original condition described by Little in 1856. Many cases follow
a premature birth and with very low birth weight.
In most cases the baby is premature by dates and some children are born
as much as 12 weeks before they are expected. Many have very low birth
weight; under three pounds and some fewer than two pounds. In some
cases the child is a twin or one of a triple. There may be a maternal history
of previous miscarriages or premature births and the birth suggests some
form of maternal inadequacy. Other premature births resulting in spastic
diplegia have followed antenatal hemorrhages in early pregnancy and also
pre-eclampsia. Spastic diplegia may follow a full term abnormal birth, or a
breech, Caesarian or forceps delivery. In the majority of cases the child was
severely ill in the neonatal period.
Spastic diplegia usually follows an abnormal birth, and in many centers the
children are on an 'at risk' register. Many have been carefully followed up
and observed. Some cases are not obviously affected in the early months
of life. They may show normal walking and placing reflexes in the neonatal
period and reciprocal kicking in infancy. The Moro reflex and the
asymmetric tonic neck reflex may be longer in evidence than is normal.
The defect is usually noted when the child is late in rolling over and in
sitting up. He is late in developing the balance reflexes in sitting, crawling
and standing.
Many of these babies are premature and their slow development is thought
to be due to this. Their milestones are delayed but postural tone is fairly
normal early on. The physiological excess of flexor tone seen in very young
normal babies may remain unaltered for many months. Although later than
normal, head control develops and the child's arms and hands seem to be
unaffected. He can get his hands together in midline and to his mouth and
he develops midline orientation of his head. His legs shown little spasticity
initially; they flexed and abducted, though full passive abduction may be
somewhat resisted. For these reasons, diagnosis is not usually made before
about 9 months of age when the child dose not sit up by him and has no
balance when made to sit. Some mildly affected children may not be
diagnosed until 18 months or even 2 years of age, when they pull
themselves, up to standing and start walking on their toes. Then they
usually show an asymmetrical pattern of standing and walking on one foot
on the toes with little weight on that leg, the other foot heel down but with
hyper -extension of the knee and flexion of that hip.
Visual: The majority of these children, even those mildly affected have in
coordination of eye movement. There is typically an internal strabismus,
but many children have difficulty in holding their eyes for a period on a
desired task. Myopia and cataracts are likely additional handicaps in a
prematurely born child.
There are 40% - 45% children are spastic quadriplegic in the total
prevalence of those with spastic cerebral palsy, all four limbs and usually
the trunk and muscles that control the mouth, tongue and pharynx are
affected. The severity of the motor impairment in Spastic Quadriplegic
implies under wider cerebral dysfunction.
Prenatal causes
These conditions are considered as high risk. Mother with thyroid disorders
Mother with mental retardation Mother with seizure disorder A lot of
studies are going on to justify the high risk factors. The specific causes of
CP spastic quadriplegic include developmental brain abnormalities, genetic
or chromosomal abnormalities, radiation exposure, prenatal infections,
illicit drug use and fetal alcohol syndrome.
Perinatal causes
Postnatal causes
The defect is usually noted when the child is late in rolling over and in
sitting up. He is late in developing the balance reflexes in sitting, crawling
and standing.
Visual: The majority of these children, even those mildly affected have
problems with co-ordination of eye movement. There is typically an internal
strabismus, but many children have difficulty in holding their eyes for a
period on a desired task. Myopia and cataracts are likely additional
handicaps in a prematurely born child.
Perceptual: Prematurely born children in particular show the visuo-motor
and perceptual defects. Before a child with spastic quadriplegia is allowed
to attend school normal or special school, the possibility of a perceptual
defect must be checked. If it is not noted the child may have extreme
difficulty with academics.
How a Child with severe spastic quadriplegia differ from a child with
less affected spastic quadriplegia?
In these children, the prognosis is bad, even when they are treated early in
life as spasticity or rigidity is already strong at a few weeks or months of
age. Epilepsy may be present early or develop later on. Fits may be of all
kinds: myoclonic jerks, petit mal, or major convulsions. May be associated
with a child's physical handicap. In some children, there are visual defects,
partial or total blindness, or visual agnostic. Hearing defects more auditory
imperceptions may also be present.
He cannot sit unsupported and falls over to one side. His back is very
round, his hips are insufficiently flexed and his legs mare too much
addicted to give him a sitting base. This combined with the asymmetry of
his spine, may produce a kypho-scoliosis.
Early, and for a long time to come, there are great feeding problems.
Tongue -thrusts are frequent as well as difficulties of sucking and
swallowing and the child may tend to choke when fed. Some children suffer
from reversed breathing, or strider and respiration present problems,
especially at night.
Even early treatment may have only limited results in furthering the child's
development. However, it can help to prevent some, if not most, of the
contractures and deformities, which quickly develop, often in a matter of
months. Treatment and advice on home management, especially in the
early stages, when we do not yet know what potential the baby may have,
are necessary to help and support the family. It helps the mother in
handing the child with greater ease and more confidence.
In babies who will later turn out to be cases of Athetosis, there is almost
invariably some concern from the neonatal period. Almost without
exception these children are difficult to feed. They may have been unable
to suck and breastfeeding may have been discontinued for that reason.
Bottle feeding may also have been difficult, and the mother gives a history
of feeding taking an abnormally long time. Chewing and swallowing
difficulties lead to problems or weaning on to solid food. In some children,
the early difficulties may have been so great that they required tube
feeding. Even for a short period this is ominous for later motor speech
difficulties. All athetoid children show delay in head control. The head is
unduly floppy. Hypotonia may last for a considerable time and is associated
with marked hypotonia of the whole body. Hypotonia lasting into the
second year may suggest an amyotonic condition; but usually the
abnormal reflex pattern, particularly of the asymmetric tonic reflex, takes
over and fluctuating spasm and tone are found.
In other athetoid children the early poor head control develops fairly
rapidly into an extensor spasm. The mother may have difficulty in feeding
the child, as whenever she attempts to feed, the child passes into an
extensor spasm. Meningitis has been diagnosed erroneously when the child
had superadded pyrexia. The mother may notice that the athetoid child
never sucks his thumb and is unable to feed himself with a biscuits or a
spoon, and never puts toys in his mouth. A study of the child shows that
this is due to the retention of the asymmetric tonic neck reflex. On the
whole it is found that the hypotonic athetoid child follows brain pathology
due to neonatal jaundice: and the hypertonic athetoid follows brain
damage due to neonatal hypoxia.
Speech: All athetoid have a very mild, mild or severe speech defect. It is a
dysarthria and may be considered as due to Athetosis of the movement of
respiration, swallowing, chewing, phonation and voice production.
A severe hearing loss may be associated with a mild motor handicap, and
vice versa.
Intelligence: It cannot be stressed too strongly that these children will very
likely have the intelligence that nature intended for them before the
cerebral insult. As the cortex is not involved in pure cases of Athetosis the
child as regards intellectual deficit is, so to speak, innocent unless proved
guilty. In fact quite a number of athetoid have a higher intelligence and
have done better educationally, than their siblings. The defect of the
inhibitory mechanism which causes the lack of control of movements may
in some way liberate the intelligence. It is in this group of cerebral palsy
cases that even when they are severely physical handicapped, there may
be high academic
For this reason all athetoid children should be assessed for education in a
school setting, and no decisions made on isolated IQ examinations.
Athetoid do not appear to suffer from the visuospatial difficulties as noted
with other groups of cerebral palsy. The incidence of educational sub
normality or severe mental sub normality may be comparatively low.
What is athetoid quadriplegia?
It was found that about 50% of cases walked before 5 years, and a further
20 - 25% before 11 years. Some cases achieve independent walking in late
adolescence, may be at 15 years of age.
Because of poor hand control, these intelligent cerebral palsied people will
not be good workers in workshops or on factory benches. It is a tragedy to
see potentially intelligent handicapped people doing the very job they are
worst at. Their education should be aimed at more intellectual pursuits
such as typewriting, proof -reading, computer programming etc. Because
of the severe physical disability many athetoid cannot be gainfully
employed. If they have educational skills such as reading they will have
much greater insight into their problems and will find it easier to adjust.
There have been many surprises, in every case because somebody had the
faith to continue with an academic education. Some of these people have
shown the maturity to make a happy marriage with another similarly
disable person. The whole of this prognosis depends on early diagnosis of
the condition of Athetosis and the determination of professionals involved
giving them the best environment for full development.
In this ill-defined group of cases there are so me, where the condition is
inherited as an autosomal recessive, and two or more in coordinated
children occur in one family. In an occasional family, the condition is
dominant and the child has the same neurological abnormality as one of
his parents. The motor disability may follow a development abnormality.
Children who survive a repair of an occipital encephalocoele may show a
true cerebellar ataxia, as part or whole of the cerebellum may be involved
in the defect. Several of these children have hydrocephalus due to a
congenital abnormality, perinatal brain damage or later cerebral infection.
An abnormal birth with severe neonatal difficulties appears to be a factor in
the causation of ataxia, as in other movement defects. Forms of ataxia
have followed various forms of meningitis or viral encephalitis.
Ataxic children may show all the additional defects of other cerebral
palsied children -
Speech: All ataxic have a very mild, mild or severe speech defect.
Due to Hypotonia, the movement of respiration, swallowing, chewing,
phonation and voice production can be affected. Hearing: There is a strong
likelihood of a partial hearing defect which takes the form of a high
frequency loss. Visual: A high incidence of hypermetropia and myopia has
been noted in Ataxic. All children should have an eye refraction
examination early. In coordinated eye movements occur in nearly every
child Epilepsy: This occurs frequently in ataxic children. Intelligence: These
children generally have poor cognition due to visuoperceptual problem.
Some workers in the field of cerebral palsy would deny the existence of this
group of cases. The world commission on cerebral palsy felt that the
condition did exist and defined it. There are children and adults in
institutions for the mentally subnormal who are described as 'spastic' by
the staff, but who do not fit into the pattern of spastic diplegia or bilateral
hemiplegia. They tend to be generally rigid. There is co contraction of both
extensors and flexors and a type of lead pipe rigidity when passive
movement is attempted. Some of these children are profoundly subnormal
and retain this general stiffness throughout life, lying in a flexed posture
with no understanding of the world.
Some children show severe retardation and general stiffness, but with
physiotherapy or persistent stimulation the rigidity may be overcome and
the child later become able to walk and use his hands. This early rigidity is
in marked contrast to the Hypotonia shown by some mentally subnormal
children.
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What are the common causes of CP rigidity?br>
CP Rigidity children may show all the additional defects of other cerebral
palsied children -
Speech: All children with CP Rigidity have a very mild, mild or severe
speech defect. Due to rigidity, the movement of respiration, swallowing,
chewing, phonation and voice production can be affected.
Intelligence: These children generally have good cognition but due to poor
hand function they are considered as mentally subnormal.