Cerebral Palsy (Its ENOUGH to study it from here)

Definitions:

Impairment:Any loss or abnormality of psychological, physiological, or anatomical structure or function.

Disability:Where an impairment causes restriction of the ability to perform any activity in the normal manner or a manner considered to be with in the limit of normality.

Handicap:Impairment or disabilities that limits or prevent the achievement of a role that is normal for that individual.

Cerebral Palsy:Non progressive lesion-sustained- wit in the immature growing brain which cause impairment of Mainly the motor function & posture. The injury develop in fetal or early life (1st 2 year of life) & it become obvious by the 5 years of age.Exclude :-lesions occur in older children, spinal cord lesion, progressive disorder of the brain e.g degenerative brain disease.

==================Etiology:

1-Prenatal 40% Genetic –AR & AD- Congenital cerebral malformation e.g Failure of migration of gray cells, Tubal

defect, Cong. Cyst, Cong. Absence of the pyramidal tract. Teratogenic e.g Alcohol Cong. Infection -TORCH- Maternal PKU

2-Perinatal 55% I.C.H Peri-venticular Leukomalaccia Birth asphyxia Cerebral artery infarction

3- Postnatal 5% Kernicterus Meningitis Hypoxic ischemic injury Cerebral traumatic injury Metabolic (HyperNa –Hypoglycemia) Status epelipticus Asphyxia

N.B:1-Most common cause of CP is Idiopathic!

Risk Factors: IUGR Prematurity 80:1000 Infants of B.wt below 1500g ==because it may cause

I.V.Hg== 1:1000 B.wt above 2500

Sever birth asphyxia Kernicterus Feeding difficulties (Nasogastric Feeding)

Association with CP:

MR 50%. Epilepsy 25% (Athetoid CP & sever insult). Hearing impairment with Athetoid CP –Kernecterus-. Cortical Blindness. Balbar palsy??? : Drooling & difficulty in feeding which may lead to

malnutrition ,dehydration, & Aspirating Pneumonia Recurrent Infection: Due to Aspirating Pneumonia & long recombinant in bed (Not Due to immunity problems!!!) Contractions: worse presentation cause it limits the child & the mother. And,

in sever case it may lead to hip dislocation. Some times due to the severity of spasticity & long recombinant in bed it may

cause osteoporosis. –Oral Q- e.g Seraj

Classifications:1- Spastic 85%

(hypertonic)-Increase in DTR- Babeneski- clonus. Diplagia 20%, Heme-, Mono-, Para-, Qaudr-35% -Most common Type is Diplagic-?2-Choreo athetotic 9%

It’s a basal ganglia lesion.It include: Increase DTR- Movement of big muscles- Not a persistent feature cause after while it will be over come by spasticity- To diffrencaite between it & chorea: In chorea it occurs when they start moving e.g stating to write or starting to comb their hair.

3-Unclassified 3%4- Hypotonic 2% To differentiate between it & LMNL you will find Hyper-reflexia (Increase DTR) 5 -Mixed.

1-Pyramidal (Asymetrical Tonic Reflex, babenski, Hypertonia, Increase DTR)

2-Extrapyramidal (Hypotonia)======================

N.B:Tetraplagic: 4 limbs either equal or UL<LLParaplagic: LLHemiplagic: 1/2 body. UL<LLDiplagic:4limbs LL<UL

Triplagic: 3 limbsMonoplagic: One limbDouble Hemiplegics: Both side of the body, where one side is affected more than the other.

========================Clinical picture:

In general: Spasticity. Increase the Tone : Clasp knife (Indicate lesion motor cortex or pyramidal) Increase DTR +/- clonus Extensor planter responses.

Symptoms:Arousal problems:

Irritability. Sleep disturbance. Lethargy. Inconsolable crying.

Feeding problem: Sucking problem Refused to feed Choking Drooling Spits

Signs: Accidental or during investigation. Failure M.S or delayed (Gross: walk, stand, sit, stand) (Manipulation:

Transfer, Holding, reaching) Persist primitive neonatal reflexes e.g (Early) Moro<6moths, Grasp<4moths. Abnormal posture or muscle tone e.g Stiff, persistence of fisting beyond age

2 months.

Non Motor Problems:1-Behaviour/psychiatric disease :sleep disturbance, irritability, & recurrent screams attacks)2-Visual problems: decrease in acuity 30%, squent, optic atrophy, myopia.3- Hearing: sensory neural deafness.4-Recurrent chest infection.5-MR 6-Epilepsy(60% in bilateral Hemiplagia)7-Educational problem.8-Speech problems: Balbar palsy & incoardination of the tongue.9-GIT : *Drooling due to balbar palsy **Constipation due to immobility & hypotonia) *** regurgitation & vomiting due to balbar palsy & GER / Hiatus hernia

I. Spastic Hemiplasia:85%Cause: Asymmetrical damage to the motor control area of only ONE hemisphere with involvement of the contra lateral side of the body.

Presentation: Obvious at age 6 months. -Signs of hemiparesis. Which include the presence of one hand that is

fisted. -Decrease the flopping or increase the tone of one wrist when th ULs

are getting shaken. -Extra beats of clonus.

Early in infancy: Failure to develop protective response of the lateral propping. Asymmetrical Parachute response (سؤال) Uneven crawling.

Early childhood: Delay walking to 2Y&1/2 TO 3 Y. Run posturing the U.L in flextion & internal rotation.

Late childhood: Arm held close to the chest in a position of adduction, flexion, internal

rotation, Leg adducted at the hip. Particularly flexed at the Knee & The Foot planter flexion.

Scliosis. Face Normal In Rt. Side hemiplagia of Post Natal origin ===< Speech is affected. BUT

NOT in congenital origin as the speech center from the other side will take over.

Convulsions are common. MR-/+

II. Spastic Diplagia:

Cause Due to Symetrical Bilateral cerebral lesion mainly corticospinal tract to

the LL. All 4 limbs LL< UL (Symmetrical involvement) Premature CP Intelligent is Normal Convulsion -/+

III. Spastic Quadriplegia-double hemiplagia:Cause: Sever & extensive injury to motor pathway in both hemisphere, MAY involve

other areas of the brain. Asymmetrical. Athetoid movement -/+ MR is sever. Convulsion -/+ Speech & swallowing are severely affected.

IV. Atheosis:Dyskinetic Abn. Of the basal ganglia. As in case of Kernectrus (Uncong. Bilirubin) pass BBB & deposit/ destroy

the Basal ganglia. Present late at age 3 years. Intelligent is NORMAL Speech : Dysarthria Deafness Convulsion is Rare.

V. Ataxia:RareCause:

genetic is rare. Aquired defect of cerebellar function.

C/P: Arms-interfere with movement. Legs-unsteady tremulous gait. If ALL limbs are involved LL<UL +ve Nystagmus +ve intention tremors. It Improve with age.

================== Diagnosis:

1. Can NOT be Dx at birth as the nervous system is Not mature enough for clinical signs to be manifested.

2. Spasticity from the background of hypotonia3. Increase DTR4. Persistence of primitive reflexes.5. Delay Developmental M.S- Gross Motor : grasp & walk.

1-Spasticity from the background of hypotonia.Increase the Tone between 12-18 months. Clear spasticity at age 2 years.1st L.L Hypertonia:A. *spasm of the hamstring Ms.

*Thigh flexed on the Abd. *Limbs extended. *Angle of the knee joint is measured. B. LL adductor Ms.When held in an upright position with the legs off the couch--< Scissoring due to Increase adduction tone

2nd U.L Hypertonia: -Usually follow LL. -Persistent adduction of the thumb into the palm of the hand "Fisting"

2-Persistence of primitive reflexes.(Early sign of CP)A- Obligatory asymmetrical tonic reflex after 6 month, if the head is turned & held for 30 sec.-Normally: Limbs from occipital side get in flexion position & those from chin side get into extension {Up to 6-8 m}, but baby can change his position.-In CP: Baby is crying & unable to change "spastic & athetoid if <6moths.

N.B: When Ex the tone in CP, we should keep the head central. Because, asymmetrical tonic neck reflex may give false impression.

B- Persistent Moro reflex < 6 mC- Persistent of grasp reflex < 4 m

3-Delay Developmental M.S- Gross Motor : grasp & walk.- walking : *Mild CP can walk at normal age.*Asymmetrical wearing out of shoes at a faster rate than normal.-Hands:* Hands move in one piece like a mechanical grabber.*Flap the hand rapidly leads to exaggeration of diminished movement of spasticity.

======================== Features of sever spastic CP:1-Limb hypertonia. - (Delayed neck support)2-crossed adductor reflex after 6 months(Test for knee jerk show adduction of the opposite thigh)3- Crossed knee reflex.

===================

Signs To exclude CP: Sensory loss. Skin lesions. Hepatomegally Eye disorder. Progressive enlargement of the head.

To diff. Between CP & Degenerative brain disease:CP:-

Delay Developmental M.S secondary to a lesion (Not a brain disease). Defect is mainly MOTOR (UL & LL) Hypertonia, Hyperreflexia, contraction.

Degenerative brain disease: Child can be initially normal. Then start to LOOS acquired M.S. It involve every thing –ALL-(Motor, Sensory, Visual, Fine, Speech)

Most –Clinical- Diagnostic feature of CP:

1-UMNL (NEVER say LMNL in CP)2-Spastic. 3- DELAY Developmental M.S (The child WON'T loose unless there is a contraction) i.e The child can even start walking at the age of 14 years!!!.4-persestant of primitive reflexes.5-Hx. Of insult.6- Your Dx should be made AFTER 6 moths, to make sure all the primitive reflexes have disappeared.7- If the child is 1 year old. On Ex. You found Head lag. It Maybe:

A-Delay MS = CP. OR B- Hypotonia To differentiate between the A & B, Do Ventral suspension.

The child will try to raise his head. So, we look to which level is the head & we compare it with the age. (Hyperextension of the Neck + Ext. & Add. Of the thighs)

N.B: Always do ventral suspension No mater how old is the child======================

The main 3 differentiation between Hypotonia & CP:1. Ventral suspension.2. Delay MS(Hx)3. UMNL

====================== E.g:18 months old child. -Can't walk-

Ask the mother : when did he sit? With or without support? If she said : At 6 months, We will ask more to know when was the

insult (Trauma, meningitis..ect) If she said : He sat 2 months ago i.e at 16 months of age, We will tell

her that he WILL walk, but after a while==========================

Early signs of CP:1. Hypertonic Neck (Ventral suspension)2. Fisting.3. Scissoring.

=============================

Management:Team work. For the child & the family.1st evaluation 2nd re-assessment.

Multi disciplinary child development center: Physiotherapist: To achieve max. potential early to facilitate normal

movment & to teach mother. Occupational Therapist: To help him to sit in position of Max

advantage to eye & head control….AND to minimize the spinal curve. Specialist health visitor Psychologist Speech therapy Social worker Dentist Orthopedic ( Release Tendon achillis to stabilize hip joint) Pediatrician who can lead with pt. & family

===================

Prognosis In sever CP----death due to recurrent infection. 50% By age 10years. Mild Cp----Good prognosis.

================= Important Hx points in CP:

Delay MS. Associated problems./ Admit for Exam on regular plan :p S/R : 1. Related to feed-growth parameters-velocity of growth i.e Increase in Wt.2. GIT: Anorixai –N/V- Diarrhea3. Resp:Chest Infection.4. CVS: In extreme malnutrition==< Dehydration & Tachycardia.5. GU: UTI6. M.sk: deformities- skin lesions & ulcer i.e bad hygiene- NB : IF convulsion you have to look for skin lesions to R/O N.F, T.S, Sturge

web Syndrome i.e neurocutaneous disease.!! PMHx: previous admissions, Frequency of admission & was it for adjust

medication or NGT. OR chest infection. Anti-pre-post natal Feeding : before how?, Now how?, balbar palsy Sx. Vaccine- Social-FHx

*==================================*N.B:This Sheet is done from Dr. S.M Jaber's Sheet & Session (Pager # 2511)-Its ENOUGH to study CP from HERE