Cerebral Palsy CEREBRAL PALSY - PowerPoint Presentation

Slide1

Cerebral Palsy

Slide2

CEREBRAL PALSY

Diagnostic

term

used

to

describe

a

group

of motor

syndromes

resulting

from

disorders

of

early

brain

development

.

Symptom

complex

, (not a

disease

)

that

has

multiple

etiologies

.

Slide3

Brain

damage

Occurs

during

developmental

period

Motor

dysfunction

Not

Curable

Non

-

progressive

(

static

)

Any

regression

or

deterioration

of motor

or

intellectual

skills

should

prompt

a

search

for

a

degenerative

disease

Therapy

can

help

improve

function

Slide4

CP is caused by a broad group of Developmental Genetic Produce a common Metabolic group of neurologic phenotypes Ischemic Infectious Other acquired etiologies

Slide5

CP is

associated

with

Epilepsy

Abnormalities

speech

,

vision

,

intellect

Selective

vulnerability

of

the

brain’s

motor

system

Many

children

and

adults

function

at a

high

educational

level

Slide6

There are 2 major types of CP, depending on location of lesions:

Pyramidal (Spastic)

Extrapyramidal

There is overlap of both symptoms and anatomic lesions.

Slide7

Types of brain damage

Bleeding

Brain malformation

Trauma to brain

Lack of oxygen

Infection

Toxins

Unknown

Slide8

Etiology

Antenatal

factors

causing

abnormal

brain

development

Congenital

anomalies

Intrapartum

asphyxia

Intrauterine

exposure

to

maternal

infection

Multiple

births

Lowbirth

weight

infants

Intracerebral

hemorrhage

Periventricular

leukomalacia

Slide9

Hypoxic Ischemic Encephalopathy (HIE)

A clinical entity first described in 1976

Used interchangeably with Neonatal encephalopathy.

Asphyxia refers to the first minutes after birth (low Apgars and acidosis)

HIE signs and symptoms persist over hours and days that follow.

Slide10

Hypoxic Ischemic Encephalopathy (HIE)

3 major lesions arise from HIE

Periventricular

Leukomalacia

(PVL)

Typically seen in the

premature infant

a. Hemorrhagic PVL

b. Ischemic PVL

Parasaggital

Cerebral Injury

Typically seen in the

term infant

Selective (Focal) Neuronal Necrosis

Seen in both

term and premature infants

Slide11

Periventricular Leukomalacia (PVL)

Hemorrhagic PVL

Periventricular

venous congestion (swelling)

may

occur, and cause ischemia (lack of blood supply) and

periventricular

hemorrhagic infarction.

Slide12

Periventricular Leukomalacia (PVL)

Ischemic PVL

An ischemic infarction or failure of perfusion usually to the watershed area surrounding the ventricular horns- “HIE white matter necrosis”.

Peak incidence occurs around 32 weeks

Larger infarcts may leave a cyst

Secondary hemorrhage can occur into theses cysts- “

periventricular

hemorrhage”.

Slide13

Periventricular leukomalacia

Slide14

Periventricular Leukomalacia (PVL)

Ischemic PVL

PVL can extend into the internal capsule and result in

hemiplegia

superimposed on

diplegia

.

Prenatal maternal ultrasound has detected lesions in the fetus at 28-32 weeks gestation, thus confirming that PVL can occur prenatally.

Slide15

Parasaggital Cerebral Injury

Injury is related to vascular factors, especially in the parasaggital border zones that are more vulnerable to a drop in perfusion pressure and immature autoregulation.

The ischemic lesion results in cortical and subcortical white matter injury.

It is usually bilateral and symmetric.

The posterior aspect of the cerebral hemisphere especially the parietal occipital regions is more affected than the anterior.

Slide16

Selective (Focal) Neuronal Necrosis (SNN)

Occurs in the glutamate sensitive areas in the basal ganglia, thalamus, brainstem and cortex.

The location of the focal necrosis, which show up as cystic lesions on MRI, depend on the stage of development of the infant’s brain at the time of the HIE.

For example, HIE at term often produces SNN in the basal ganglia since it is glutamate sensitive and very hypermetabolic at term.

Slide17

Types of Cerebral Palsy

Pyramidal Velocity dependent increased resistance to passive muscle stretchThe spasticity can be worse when the person is anxious or ill.The spasticity does not go away when the person is asleep.

Extrapyramidal

Ataxia

Hypotonia

Dystonia

Rigidity

The tone may increase with volitional movement, or when the person is anxious

During sleep the person is actually hypotonic

Slide18

Types of Cerebral Palsy

Pyramidal (Spastic)

Quadriplegia- all 4 extremities

Hemiplegia

- one side of the body

Diplegia

- legs worse than arms

Paraplegia- legs only

Monoplegia

- one extremity

Slide19

ExtrapyramidalDivided into Dyskinetic and Ataxic types

DyskineticAthetosisChorea- quick, jerky movementsChoreoathetosis- mixedHypotonia- floppy, low muscle tone, little movement

Ataxic CP

Results from damage to the cerebellum

Ataxia- tremor & drunken- like gait

Slide20

Anatomy

PyramidalLesion is usually in the motor cortex, internal capsule and/or cortical spinal tracts.

Extrapyramidal

Lesion is usually in the basal ganglia, Thalamus, Subthalamic nucleus and/or cerebellum.

Slide21

SPASTIC DIPLEGIA

Periventrıcular

leukomalacia

(PVL)

Prematurity

Ischemia

Infection

Endocrine

/

Metabolic

Slide22

SPASTIC

QUADRIPLEGIA

PVL

Multicystic

encephalamalacia

Malformation

infection

endocrine

/

metabolic

genetic

/

developmental

Slide23

HEMIPLEGIA

Stroke

inutero

or

neonatal

Thrombophylic

disorders

Infection

Genetic

/

developmental

Periventricular

hemorrhage

-

infection

Slide24

EXTRAPYRAMIDAL

(

athetoid

-

dyskinetic

)

Pathology

,

putamen

,

globus

pallidus

,

thalamus

,

basal

ganglia

Asphyxia

Kernicterus

Mitochondrial

Genetic

/

metabolic

Slide25

SYMPTOMS

All types of CP are characterized by

Abnormal muscle tone

Reflexes

Motor development

Coordination

Slide26

Classical

Symptoms

Spasticities

Spasms

Involuntary

movements

Unsteady

gait

Problems

with

balance

Scissor

walking

Toe

walking

Slide27

Babies

born

with

severe CP

often

have

an

irregular

posture

floopy

or

stiff

spinal

curvature

small

jawbone

Slide28

SPASTIC HEMIPLEGA

Decreased

spontaneous

movements

on

the

affected

side

The

arm

is

often

more

involved

than

the

leg

Difficulty

in

hand

manipulation

is

obvious

by

1

yr

of

age

Walking

is

delayed

until

18-24

months

Circumductive

gait

is

apparent

Slide29

Examination

of

the

extreminites

may

show

growth

arrest

Spasticity

is

apparent

in

the

affected

extremities

An

affected

child

often

walks

on

tiptoe

Ankle

clonus

and

a

Babinski

sign

may

be

present

DTR

are

increased

Slide30

1/3

of

patients

have

a

seizure

disorder

25%

have

cognitive

abnormalities

Slide31

CT

or

MRI

→An

atrophic

cerebral

hemisphere

with

a

dilated

ventricule

contrlateral

to

the

side

of

the

affected

extremities

CT →

Useful

for

detecting

calcifications

associated

with

congenital

infections

Family

histories

suggestive

of

thrombosis

and

inherited

clotting

disorders

may

be

present

Slide32

SPASTIC DIPLEGIA

The

most

common

form of

the

spastic

forms

Bilateral

spasticity

of

the

legs

First

indication

is

often

noted

when

an

infant

begins

to

crawl

=

commando

crawl

If

the

spasticity

is severe

application

of

diaper

is

difficult

Slide33

Ankle

clonus

,

Babinski

sign

(

bilateral

)

Scissoring

posture

of

the

lower

extremities

Walking

is

delayed

Child

walks

on

tiptoe

Impaired

growth

of

lower

extremities

Hip

problems

,

dislocations

,

strabismus

Normal

intellectual

development

Slide34

SPASTIC QUADRIPLEGIA

→ ( TETRAPLEGIA)

Most severe form of CP

Motor impairment of all extremities

High association with mental retardation and seizures

Swallowing difficulties are common

→ aspiration pneumonia

Increased tone and spasticity

Brisk reflexes, plantar extensor responses

Speech and visual abnormalities

Slide35

ATHETOID CP= EXTRAPYRAMIDAL CP

Less

common

Affected

infants

are

characteristically

hypotonic

with

poor

head

control

Developed

increased

variable

tone

with

rigidity

and

dystonia

over

several

years

Feeding

may

be

difficult

Slide36

Speech

is

typically

affected

Oropharyngenal

muscles

are

involved

Seizures

are

uncommon

Can

also

be

caused

by

kernicterus

Slide37

DIAGNOSIS

History

Physical examinaton

Neurological examination

MRI

→ determine the location and extent of structural lesions,associated congenital anomalies

Hearıng and visual function test

Genetic evaluation

Slide38

TREATMENT

Multidisciplinary approach in the treatment

Physians from various specialities

Occupational and physical therapist

Speech pathologist

Social workers

Educators

Developmental psychologist

Slide39

Parents should be taught now to work with their children in daily activities

Feeding

Carrying

Dressing

Bathing

Playing

Need to be instructed in the supervision of a series of exercises to prevent the development of the contractures

Slide40

Spastic diplegia → treated initially with the assistance of adaptive equipment such as walkers some surgical procedures that reduce muscle spasm.

Slide41

Quadriplegıa

Motorized wheelchairs

Special feeding devices

Modified typewriters

Customized seating arrangements

Slide42

Hemiplegia

Improved hand or arm functioning on the affected side

Slide43

Orthopedic Problems

Scoliosis

Hip Dislocations

Contractures

Osteoporosis

Slide44

Medical Management

Oromotor Dysfunction

Especially common in persons with Extrapyramidal CP and Spastic quadriplegia

Language delay/Speech delays

Drooling

Dysphagia

Aspiration

Slide45

Medical Management

Gastrointestinal

Dysmotility

Delayed gastric emptying

Gastroesophageal

reflux

Pain

Chronic aspiration

Constipation

.

Slide46

Medical Management

Gastrointestinal Dysmotility

Delayed gastric emptying

Gastroesophageal reflux

Pain

Chronic aspiration

Constipation

These disorders are interrelated and compound one another.

Slide47

Medical Management

Spasticity Management

Management of spasticity does not fix the underlying pathology of CP, but it may decreased the sequelae of increased tone.

Over time, the spasticity leads to:

musculoskeletal deformity

scoliosis

hip dislocation

contractures

Pain

Hygiene problems

Slide48

Treatment of Spasticity

Medications

Valium

Dantrium

Baclofen

Clonidine

Clonazepam

BOTOX

Slide49

Associated Problems

Mental RetardationCommunication DisordersNeurobehavioralSeizuresVision DisordersHearing lossSomatosensation (skin sensation, body awareness)

Temperature instability

Nutrition

Drooling

Dentition problems

Neurogenic bladder

Neurogenic bowel

Gastroesophageal reflux

Dysphagia

Autonomic dysfunction