Classifications of Cerebral Palsy

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Classiﬁcations of cerebral palsy
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In: Orthopedic Management of Children with Cerebral Palsy ISBN: 978-1-63483-318-9
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Chapter 7
CLASSIFICATIONS OF CEREBRAL PALSY
Vito Pavone* and Gianluca Testa

Department of Orthopedics, University of Catania, Italy
ABSTRACT
Cerebral Palsy (CP) is a clinical entity that encompasses different cerebral disorders.
This affection is very frequent in the general population and manifests mostly with severe
dysfunction involving several organs and districts. The dysfunction affects not only the
motor features, but also is usually associated with severe cognitive, behavioral and
communication disorders. Most of these patients do not work at all and suffer severe
cognitive delay.
For the classification of CP it is useful to compare the results and the data of
different motor impairment subgroups, the evaluation of the association of CP with the
other neurologic and psychiatric dysfunctions, the association with other non-cerebral
impairments, and the results of intervention therapies, as well as establishing the
etiological events which cause the disorder. In other words the main goal of a widely
recognized CP classification is to collect the children with the disorder into a more
homogeneous group or category of the same type to have epidemiologic results in the
different fields of this heterogeneous disorder. For 150 years, the classification of CP has
been to consider its relevant importance and address the evaluation of motor affection.
More recently, new attention has been addressed to other aspects, which involve the
disorder including etiology and timing of the presumed events, type, severity of the motor
involvement, anatomical distribution, and associated dysfunction. Together with the
classification of motor involvement and its classic differentiation in spastic, dyskinetic,
ataxic and mixed, and related forms, attention has moved to develop a classification
regarding the gross motor functions, to evaluate the bimanual fine motor activity and the
ability of patients with CP to use their hands in routine situations. A scale has been
prepared and used for the evaluation of communication, the mode of walking and
dystonic impairment.
*
Corresponding author: Vito Pavone, MD Department of Orthopedics, Azienda Ospedaliero-Universitaria
Policlinico Vittorio Emanuele, Via Santa Sofia, 78 95123 Catania, Italy; Email: vitopavone@hotmail.com

76 Vito Pavone and Gianluca Testa
Keywords: cerebral palsy, CP classification, Gross Motor Function Classification System,

Functional Mobility Scale, Manual Ability Classification System, Communication
Function Classification System, Classifications of gait analysis
KEY POINTS
 Several classification systems are available.
 Classification are useful to compare different motor impairment subgroups.
 Classification systems allow to evaluate not only walking abilities but also
communication, ability to use hands and outcome of surgery.
7.1. INTRODUCTION
Cerebral Palsy (CP) is neither a disease nor a single entity, but rather a disorder that
encompasses different cerebral disorders.
CP involves a group of permanent disorders of movement and posture causing activity
limitations that are attributed to non-progressive disturbances that occur in the developing
fetal or infant brain. CP motor disorders are often accompanied by disturbances of sensation,
perception, cognition, communication or behavior, by epilepsy and by secondary
musculoskeletal problems.
In the definition, the term CP includes: 1) motor involvement; 2) cerebral origin of the
lesion; 3) no progression; 4) precocious involvement of the Central Nervous System (CNS) 5)
frequent association with other neurologic and behavioral disorders. In the CP definition there
is no general agreement as concerns the upper limit for age at onset, and the inclusion criteria
to categorize syndromes, genetic disorders, or brain abnormalities presenting as non-
progressive CP.
CP is the most common cause of chronic disability in childhood occurring in 2 to
2.5/1000 births and is a severe disorder since a significant number of patients may present
cognitive delay and impossibility to walk without support. As the disorder involves different
clinical aspects, an interdisciplinary set of professionals is implicated to care for the affected
patients including pediatricians, pediatric neurologists, orthopedic surgeons, child
rehabilitators, occupational therapists, ophthalmologists, otorinolaryngologists, geneticists
and other specialists.
William Little, an English orthopaedic surgeon, is generally credited with the first
description of CP and the related musculoskeletal issues in one of a series of lectures, entitled
“Deformities of the Human Frame,” carried out in 1843. Subsequently, as reported by Morris
scarlet fever and vaccinations were indicated as the main causes of the disorder [1].
7.2. ETIOLOGY
Cerebral palsy CP is caused by an alteration of the CNS in the early stages of
development: during pregnancy, at birth or during the first 2 years of postnatal life, but the

Classifications of Cerebral Palsy 77
limit of this last point is debated. The clinical presentations depend on the severity and extent
of the damage and its location (brain, brainstem or spinal cord). The severity of the signs and
symptoms therefore may vary from a mild to severe motor impairment, associated with
different systemic involvements.
Relevant maternal predisposing factors are familiarity for CNS disorders and chronic
maternal diseases, such as diabetes, epilepsy and mental retardation. Among the risk factors
related to pregnancy are: (before pregnancy) frequent episodes of abortions and prolonged
menstrual cycles; (during pregnancy) social conditions, threats of abortion, bleeding at
various stages of pregnancy, preeclampsia, hypertension, and placental abnormalities
(especially placental vascular anastomoses and amniotic membranes), placental detachment,
multiple pregnancies and fetal infections, intrauterine growth retardation and prematurity;
(during birth) fetal malposition, maternal vaginal infections. In addition, it is well established
that the risk of developing CP increases with low gestational age and weight of the baby when
it is less than 2500 g. This risk increases 20-fold in infants weighing less than 1500 g. factors.
Congenital infections of the TORCH complex, neonatal bacterial, viral and fungal infections
have decreased in recent years in developed countries, as well as the outcomes of neonatal
icterus, which in the past caused Kernicterus, due to severe impairment of the basal ganglia.
On the other hand, the survival of prematures and newborns with low weight under 1500 g
has indirectly caused an increase of individuals with CP [1].
Genetic forms of CP have been more recently outlined. Hereditary spastic paraplegia
(HSP) encompasses a group of disorders characterized by muscle weakness and spasticity
with insidious onset and progressive course. HSP are distinguished in "uncomplicated” and
“complicated” forms. In the first the spasticity is progressive mainly involving posterior
muscles of the thigh and of the quadriceps, ileopsoas and anterior tibialis and dysfunction of
the bladder is often associated. Complicated HSP, further to the above mentioned signs and to
other neurologic manifestations (not imputable to syndrome neurologic features), manifests
with seizures, intellective delay, ophthalmologic dysfunction and hearing disorders. However,
due to their progressivity HSPs are usually not included in the classic group of CP but these
forms, together with multiple monogenic syndromes that manifest clinical features of CP,
should be considered in the diagnostic evaluation of CP.
Other Genetic Factors. Multiple genetic factors have been reported in association with
CP as demonstrated by: a) a higher concordance rate for CP in monozygotic twins compared
with dizygotics; b) the risk of CP in consanguineous families (2.5 times higher); c) the higher
frequency of familial CP affected patients compared with the general population. Mutations
in multiple genes and several new single gene mutations have been associated with CP.
Recently Moreno-De Luca reported genes etiologically related to CP: glutamate
decarboxylase I (GADI); the KN motif and ankyrin repeat domain I (KANKI); adaptor-
related protein complex 4, mu I subunit (AP4MI); adaptor-related protein complex 4, epsilon
I subunit (AP4EI); adaptor-related protein complex 4, beta I subunit (AP4BI); adaptor-related
protein complex 4, and sigma I subunit (AP4SI [2]).
Causal factors of CP include environmental conditions, gene anomalies, metabolic
dysfunctions (particularly severe hypoglycemia and hypocalcaemia), intrauterine teratogens,
viral, bacterial and fungal infections, traumatic delivery and hypoxic ischemic
encephalopathy. The last one is one of the most frequent causes of perinatal brain damage.
Neonatal cerebral dysfunction determines various disorders with different grades of severity:
a) cognitive manifestations which manifest with language, difficulty in solving problems, low

intellective verbal and non-verbal quotient, memory deficit; b) voluntary and involuntary
motor movement anomalies, CP, anomalies of the tonus, strength and reflexes,
incoordination, and anomalies of graphomotor capacity; c) neurobehavioral manifestations
including attention deficit, poor control, deficit in social interaction, aggressivity; d)
neuroanatomic and neurophysiologic manifestations such as microcephaly, macrocephaly,
structural cerebral anomalies, and seizures [1].
In conclusion the risk factors significantly associated with CP include placental
abnormalities, major and minor birth defects, low birth weight, meconium aspiration,
emergency caesarean section, birth asphyxia, neonatal seizures, respiratory distress syndrome,
hypoglycemia, and neonatal infections.
Pathophysiology. CP is caused by non-progressive and permanent injuries that affect the
motor cortex within the first 2 years of life. There is a higher cortical damage to motoneurons
(first motor neuron) with a decrease in excitatory and regulator input from the cortex through
the reticulo-spinal and corticospinal tracts to reach motoneurons of the brain stem and spinal
cord (second motoneuron) that control the peripheral muscle groups. This decrease of input
interferes with motor control, reducing the number of motor units and causing muscle control
deficit and weakness. Moreover, the loss of inhibitor descendant inputs, mediated by the
reticulo-spinal tracts and from other systems, results in increasing excitability of gamma and
alpha-motoneurons determining spasticity, defined as a type of muscular resistance to
stretching or as excessive or involuntary muscle activity. Spasticity could determine
complications associated with CP, such as contractures, pain and subluxations. Spasticity is
also worsened by primary or secondary complications of the spinal cord, such as alterations
of nociceptive inputs. The elimination of the spastic component allows many individuals with
CP to be able to use more effectively and functionally the residual component of selective
motor control [1].
The damage to the extrapyramidal system causes movement disorders such as athetosis,
chorea, dystonia, or rigidity. Diplegia is associated with periventricular leukomalacia,
hemiplegia with lesions in a single hemisphere and quadriplegia with multiple lesions.
Therefore type and extension of damage to the CNS, the location of the insult (which is
irreversible) and the capacity for adaptation and reorganization of the CNS, after suffering the
injury, regulate the type and severity of clinical presentations and natural history of
neurological deficits in CP [1].
7.3. DIAGNOSIS
In the field of CP it is necessary to have a correct familial anamnesis, the normal or
abnormal course of the pregnancy to try to establish the timing of the pathological events, an
early diagnosis, and what caused the brain impairment in the child. The diagnosis must be
performed through a physical and neurological examination, extended to the other body
organs that could possibly be affected. Laboratory analysis, include a test for pre- or post-
natal infections, and neuroimaging investigations, including neonatal cranial ultrasound, and
cerebral tomography or Magnetic Resonance Imaging. In specific cases it is worthwhile to
perform a molecular analysis.

Early diagnosis and specific causes in CP patients are worthwhile both for obtaining a
rapid and useful medical treatment and therapeutic interventions and avoid recurrence risk
and also to allow the family to better face the problem. There are anamnestic and clinical
signs that can help to recognize an early onset CP: a) personal history (prematurity, neonatal
encephalopathies (hypoxic-ischemic encephalopathies, neonatal seizures, stroke); b)
ultrasound investigation in prematures who show intraventricular hemorrhages, cystic lesions
of the White Matter, ventriculomegaly and in newborns who show dorsal ganglia, thalami and
posterior quarter of internal capsula anomalies; at the physical examination in the subsequent
months, the patients present hypotonia, muscle weakness, motor incoordination and
asymmetry, abnormal archaic reflexes, tardive postural responses. Functional limitations
consist of anomalies of motor age/chronologic age ratio, anomalies of movements which are
asynchronous and reduction or absence of active movements of limbs, neck and trunk. The
International CP Task Force gave this indication to define an acute intrapartum hypoxic event
[3]. Essential criteria: a) evidence of metabolic acidosis in intrapartum fetal, umbilical arterial
cord or very early neonatal blood samples (pH < 7.00 and base deficit >12 mmol/l; b) early
onset of severe or moderate neonatal encephalopathy in infants of more than 34 weeks
gestation, c) CP of the spastic quadriplegia or dyskinetic type. The Task Force suggested
further indications of an acute intrapartum hypoxic event registered as non-essential criteria
or additional criteria: a) a sentinel (signal) hypoxic event occurring immediately before or
during labor; b) a sudden, rapid, and sustained deterioration of the fetal heart rate pattern
usually after the hypoxic sentinel event when the pattern was previously normal; c) Apgar
score of 0-3 minutes longer than 5 minutes; d) early evidence of multisystem involvement:
and e) early imaging of acute cerebral abnormality.
Figure 1. Left hemiparesis in an 18 month old boy. The right foot is internal rotated to maintain walking
position.

Figure 2. Hyperextension of lower limbs following suspension maneuver
Figure 3. CP in a 2 year old boy. Notice hyperextension of lower limbs with scissoring feature.
Figure 4. Equinus-varus foot with severe hypotonia in a one year old child.

Figure 5. Scissoring feature of lower limbs.
Figure 6. Spastic quadriplegia with sever involvement of the upper limbs.
Figure 7. Rigid Spasticity in a six month old boy with severe brain damage.

Relevant importance for a correct early diagnosis is the use of neonatal cranial ultrasound
and cerebral MRI. Neonatal brain damage could be shown by Periventricular (PVL)
anomalies which are subdivided into different grades of severity: 1) grade I, areas of
increased echogenicity, usually seen after 24-48 hours after the insult and persisting beyond
day 7, but not evolving into cysts; 2) grade II, localized small cysts, often located in the
fronto-parietal periventricular white matter; 3) grade III, extensive cystic lesion, often
particularly prominent in the parieto-occipital periventricular white matter. The cysts usually
do not communicate with the lateral ventricle. They usually collapse after several weeks and
are no longer visible on US at 2-3 months. At this stage, irregular ventricular dilation can be
seen due to the atrophy of the periventricular white matter; and 4) grade IV, extensive cystic
lesions extending into the deep (subcortical) white matter [3].
MRI signs of antenatal insult or development abnormality, in the classification proposed
by Cowan are: irregular ventricular dilatation, widening of the interhemispheric fissure,
enlarged extracerebral space; established cystic lesions: porencephaly, germinolytic cysts,
cystic periventricular leucomalacia; focal infarction with atrophy; longstanding hemorrhage;
marked asymmetries (i.e. in ventricular shape or size, hemispheric size, cerebellum, brain
stem, or operculum); developmental anomalies (i.e. in cortical dysplasia, midline structural
anomalies, abnormal cerebellar development) [4].
MRI signs of acute perinatal insult are: brain swelling; cortical highlighting; focal or
global loss of grey-white matter differentiation; abnormal signal intensity in the basal ganglia
and thalami -typically the posterior putamen and ventrolateral nucleus of the thalamus
(VLNT) but could include the caudate nucleus and globus pallidus; loss of normal signal
intensity in the posterior limb of the internal capsule (PLIC) associated with the above
cortical, white matter or basal ganglia and thalami abnormality; acute and subacute
parenchymal, intraventricular, or extracerebral hemorrhage; acutely evolving focal infarction
in an arterial territory or in a parasagittal or watershed distribution [4].
Figure 8. Severe brain suffering with extensive cystic areas.

The physical and neurological examination is related to identify the muscle tone, the
hypo or hypertonia and the predominant type of motor impairment and the unilateral or
bilateral limb involvement. A diagnosis of CP is difficult prior to 1 year of age unless it is
quite severe. Due to the progressive maturation of the CNS, the infant will present sequential
changes in the clinical picture and in the first months of life it is frequent to notice a
hypotonic muscle state instead of hypertonia which will possibly develop later. Also the
dyskinetic movements as the choreoathetoid type will become evident only after 1 year of
age. In fact, during the first months of life, the motor function of an infant is based primarily
on archaic reflex with reflex arc being caudal to the cerebral cortex.
Figure 9. Periventricular brain cyst secondary to hypoxic-ischemic injury.
Figure 10 (A-C). Periventricular cystic lesions and wide damage of lateral ventricles.

The clinical examiner should assess tone, deep tendon reflexes, and primitive reflexes to
try to notice motor dysfunction. After the second semester the classic signs of upper motor
neuron dysfunction became clearer: hypertonus and hyperreflexia became more evident as
well as differentiation between spasticity and rigidity. Athetosis and ataxia may be recognized
at the age of 1 and ½- 2 years of age. Sometimes, at around 4 months the parents of a child
speak to their pediatrician having noted that one of the infant’s hands will remain fisted
differently from the other; this can be an early sign of hemiparesis. Another sign is reported
by parents referring that the baby is using only one hand in reaching out. At 6 to 7 months of
age lateral propping or support reaction reflexes are well developed and this is useful to
establish a unilateral motor dysfunction. Characteristic of the spastic type are: spastic
hypertonia, hyperreflexia with clonus, wide reflexogenic area, Babinski positive, slow
voluntary movements, anomalous fine-motor function, difficulty to perform simple
movements, and muscular fatigue.
The clinical examination should be extended to identify the various disorders which often
are associated with CP: intellectual delay, epileptic seizures, speech and language deficit,
visual impairment (strabismus, retinopathy, nystagmus) hypo-acusia, oromotor dysfunction,
and somato sensory deficit. The examination should also be extended to notice other
anomalies often present in these children: gastroesophageal reflux, spontaneous fractures,
problems with feeding, swallowing, and bowel motility, poor nutrition, stunted growth,
frequent infections, are reported with an high frequency, and behavioral problems range
between 30-60% of the individuals affected. Other reported comorbidities include,
genitourinary, gastrointestinal, respiratory and endocrine problems. However, most
complications are related to intellective delay and the presence of epileptic seizures [2].
7.4. PREVIOUS CLASSIFICATIONS

Some years later William Little in 1862, differentiated congenital deformities such as
talipes equinovarus from the acquired disorders caused by prematurity or birth damage which
subsequently involved the extremities and which he called spastic rigidity. Little is also the
author of one of the first classifications of CP as he distinguished the different forms of CP in:
a) hemiplegic rigidity mainly affecting one side but also the other side even if with less
impairment; b) paraplegia affecting both legs and arms but with less involvement of the arms;
and, c) generalized rigidity. For his wide concern on this topic, one of the types of CP,
diplegia, was indicated for several years under the name “Little’s disease.” The first
classifications distinguished three categories using the term infantile hemiplegia, bilateral
spastic hemiplegia and spastic paraplegia. The famous psychoanalyst Sigmund Freud, before
his interest in psychological problems, dedicated his studies to CP and profiting from his
knowledge in the field of neuropathology he distinguished diplegia, affecting lower limbs
bilaterally from hemiplegia involving the unilateral site. He also used the term diplegia to
encompass other categories of CP such as generalized rigidity of cerebral origin, paraplegic
rigidity, double spastic hemiplegia, generalized congenital chorea and generalized athetosis.
Phelps was one of the first to give indications for treating patients with CP suggesting
physical therapy, orthoses, and nerve blocks and suggested a classification on a functional
basis also including physical and mental impairment [5]. He also advised to use the term

dyskinesia to gather all the movement disorders and indicated spasticity, athetosis, overflow
or synkinesia, incoordination or ataxia and tremor as sub-categories. The “Little Club” a
group made up of Mac Keith and Polani in 1957 distinguished the disorders in a) spastic,
further subdivided in hemiplegia, double hemiplegia, and diplegia, and b) a second group in
which dystonia, choreo-athetosis, mixed ataxia and atonia were enclosed [5].
The group “Evans form” expanded the classification according to the involvement of the
CNS and the muscle tonus and distinguished different forms: 1) hypotonia; 2) hypertonia
manifesting with stiffness, spasticity and rigidity; 3) dyskinesia and; 4) ataxia. As regards this
topic the group recognized an important role of the functional activity and pointed out the
relevance of intellectual and sensory involvement, difficulties in communication, the presence
of epileptic seizures and the etiological factors which have caused the cerebral impairment,
such as cerebral malformations, acquired cerebral damage and genetic disorders.
A Swedish classification system categorized the disorders into neurologic basis and
distinguished three different groups: spastic, ataxic and dyskinetic and subcategorized in
mixed as hemiplegia, tetraplegia, or diplegia for spastic forms; as either diplegic or congenital
for ataxic form; and as either mainly chorio-athethotic or mainly dystonic for dyskinesic
forms [5].
In general CP was classified following various conditions: according to the anatomical
side of the brain lesions in the cerebral cortex, pyramidal tract, extrapyramidal system, or
cerebellum; clinical symptoms and signs in spasticity, dyskinesia (including dystonia and
choreo-athetosis forms) or ataxia; topographical involvement of extremities (diplegia,
quadriplegia, or hemiplegia); timing of presumed insult (prepartum, intrapartum, or
postneonatal); and classification of degree of muscle tone (isotonic, hypotonic, or hypertonic).
Classification of CP patients has been updated for several years with the aim of
characterizing the various clinical aspects, harmonizing and comparing the results of different
studies as regards etiology, treatments and prognosis of the affected patients.
The clinical presentations of patients with CP often differ for gestational age, gestational
causal events, chronological age, size of the lesion and pre-peri and post-natal etiological
factors [6].
The first classifications were based on motor abnormalities, on distribution pattern of the
affected extremities (hemiplegia and diplegia), on predominant tone type (spastic) or
movement abnormalities (dyskinesia) and according to the anatomic lesion: corticospinal or
pyramidal tract lesions (spastic form); extrapyramidal tract lesions (dyskinetic form);
cerebellar tract lesions (ataxic forms); lesions of the corticospinal or pyramidal tract (atonic
forms); mixed forms. Depending on the severity, each form was divided into minimal
(clinical signs without functional disability), mild, moderate, or severe.
To highlight this, the clinical picture is not always specific: abnormal involuntary
movements in spastic forms are observed and pyramidal signs may be present in dyskinetic
and ataxic syndromes.
Classification of CP reported by Taft [6] is based on the clinical description of the
neuromotor dysfunction and according to this Author the nosology based on clinical features
is appropriate since in many cases of CP neither pathology nor etiology are often known.
According to the motor dysfunction CP is distinguished into five groups: a) Spastic, including
subgroup hemiparesis (monoparesis), diplegia, quadriparesis (double hemiplegia); b)
Dyskinetic, including sub-groups athetoid, dystonic, chorea, ballismus, tremor; c) rigid; d)
ataxia; e) mixed (Table 1)

Table 1. Clinical classification of CP based on clinical description [7]
Type of impairment
Spastic
Hemiparesis (monoparesis)
Diplegia
Quadriparesis (double hemiplegia)
Dyskinetic
Athetoid
Dystonic
Chorea
Ballismus
Tremor
Rigid
Ataxic
Mixed
From Taft, 1995
In April 2001 an interdisciplinary workshop was held at the National Institutes of Health
by the Task Force on Childhood Motor Disorders with the aim of classifying and defining the
disorders causing hypertonia in childhood.
The Definitions concerning the term “spasticity,” “dystonia” and “rigidity” [8]. From this
workshop the definition of the term “Spasticity” is defined on the presence of one or both of
the following signs: 1) resistance to externally imposed movement increases with increasing
speed of stretch and varying with the direction of joint movement, and/or 2) resistance to
externally imposed movement rising rapidly above a threshold speed or joint angle. The term
“Dystonia” defines a movement disorder in which involuntary sustained or intermittent
muscle contractions cause twisting and repetitive movements, abnormal postures, or both.
The definition of “Rigidity” is a hypertonia in which all of the following are reported: 1) the
resistance to externally imposed joint movement is present at very low speeds of movement,
does not depend on imposed speed, and does not exhibit a speed or angle threshold; 2)
simultaneous co-contraction of agonists and antagonists may occur, and this is reflected in an
immediate resistance to a reversal of the direction of movement about a joint; 3) the limb does
not tend to return toward a particular fixed posture or extreme joint angle; and 4) voluntary
activity in distant muscle groups does not lead to involuntary movements about the rigid
joints, although rigidity may worsen.
A new consensus was made at the National Institutes of Health in Bethesda, Maryland in
2005, concerning the definition and classification of negative motor signs in childhood. As
reported by Sanger et al. [8], a previous general classification of motor signs basically
distinguished two categories: positive signs and negative signs. The definition of positive
motor signs includes those motor signs that lead to involuntary increased frequency or
magnitude of muscle activity, movement or movement pattern. Examples of this group of
motor dysfunctions are hypertonia, chorea, tics and tremor. Negative motor signs include
insufficient muscle activity or insufficient control of muscle activity and were categorized
into 4 groups: 1) insufficient muscle activation (weakness); 2) inability to activate a specific
pattern of muscles (reduced selective motor control); 3) inability to activate the correct
pattern of muscles during movement (ataxia); and 4) inability to activate the correct pattern of

muscles to accomplish a task (apraxia and developmental dyspraxia). The negative motor
signs were given this definition [8]: “Weakness” is reported as the inability to generate
normal voluntary force in a muscle or normal voluntary torque about a joint; “Reduced
selective motor control” an impairment in the ability to isolate the activation of muscles in a
selected pattern in response to demands of a voluntary posture or movement; the term
“Ataxia” is referred to an inability to generate a normal or expected voluntary movement
trajectory that cannot be attributed to weakness or involuntary muscle activity about the
affected joints and; “Apraxia” an impairment in the ability to accomplish previously learned
and performed complex motor actions that are not explained by ataxia, reduced selective
motor control, weakness, or involuntary motor activity; and “Developmental dyspraxia” is
defined as a device to define a failure to have ever acquired the ability to perform age-
appropriate complex motor actions that were not explained by the presence of inadequate
demonstration or practice, ataxia, reduced selective motor control, weakness, or involuntary
motor activity.
More recent classifications of CP are essentially based on the: 1) type and severity of
the motor abnormalities; 2) anatomical distribution of the involved extremities; 3)
characteristic of the neurological associated dysfunction. and 4) timing of the presumed
causal event. Although CP as a disorder has been known for one and half centuries,
nevertheless, no agreed method of classification has been universally accepted, also in
consideration of the frequent new insights which occur in this field of research.
The Surveillance of CP in Europe (SCPE) [9, 10] network started in 1998 and
developed collaborative studies in the following years with the aim of homogenizing CP data
collection using a standard definition, developing a central database of children with CP in
order to monitor trends in birth weight, specific rates and organizing collaborative research.
SCPE classified the patients with CP according to classes or categories of the same type,
into three main groups, spastic, dyskinetic and ataxic, based on neurological signs, indicating
lesion in the cerebral motor systems. (Table 2)
According to SCPE, CP subtypes share an abnormal pattern of movement and posture:
patients with A) spastic CP show increased tone, pathological and abnormal reflexes. The
pathological posturing of lower limbs is observed by: 1) internal rotation of the hip; 2) hip
adduction; and, 3) equinus foot, resulting in a scissored position. B) Dyskinetic patients show
involuntary, uncontrolled, recurring and occasionally stereotyped movements, the primitive
reflex pattern predominates and muscle tone is varying: dystonic and athetoid CP are used as
subtypes for subgrouping ; C) ataxic children show loss of orderly muscular coordination and
movements are performed with abnormal force, rhythm and accuracy: ataxic movement in CP
is characterized by 1) loss of orderly muscular coordination with movements carried out by
increased force, rhythm, and accuracy; 2) tremor; 3) and low tone; D) the mixed CP type
spasticity with ataxia and/or dyskinesia, is defined according to the prominent clinical feature.
Furthermore, the SCPE network recommends the collection of data with the association
of CP with other clinical abnormalities (intellectual delay, visual and hearing impairments
and epilepsy). SCPE recommends, moreover, the scoring of motor function according to the
Gross Motor Function Classification System (GMFCS) for motor functions and Bimanual
Fine Motor Function (BFMF) for the upper limbs giving the chance to reveal possible
asymmetry in hand functions. For further training tools SCPE advice the use of written
classification guidelines with video description of children with CP.

Table 2. SCPE Classification of CP
Spastic CP Increased tone and abnormal reflexes.

Dyskinetic Involuntary, uncontrolled, recurring and occasionally
stereotyped movements.
Ataxic Loss of orderly muscular coordination, movements are
performed with abnormal force, rhythm, and accuracy.
Mixed (spastic type with ataxia According to the dominant clinical feature.
and/or dyskinesia)
From Cans et al. 2007
The application of the system advised by SCPE with application of inclusion/

exclusion/classification criteria has reached these results: a four-fold increased risk of CP in
multiple births has been noticed, mainly explained by gestational age distribution; a
decreasing trend of infections as cause of post-neonatal CP patients; an optimal birth weight
associated with a lower risk of CP, and a decreasing CP prevalence in children with a birth
weight between 1000 and 1500g [10].
The Executive Committee for the Definition of CP (ECDCP) advanced a classification
(Table 3), following these aims: a) description with a level of detail that will clearly delineate
the nature of the problem and its severity in a single individual; b) prediction, collecting of
information about health care professionals of the current and future service, needs of affected
individuals; c) comparison of patients affected by CP assembled in different places; d)
evaluation of change to allow comparison of the same individual with CP at different points
in time.
Table 3. Components of CP classification (ECDCP)
Motor abnormalities A. Nature and typology of the motor disorder. The observed tonal
abnormalities assessed on examination (e.g. hypertonia, hypotonia) as
well as the diagnosed movement disorders present such as spasticity,
ataxia, dystonia, athetosis.
B. Functional motor abilities. The extent to which the individual is
limited in his or her motor function, including oromotor and speech
function.
Accompanying The presence or absence of later-developing musculoskeletal problems
impairments and/or accompanying non-motor neurodevelopmental or sensory
problems, such as seizures, hearing or impairments that interact in
individuals with CP.
Anatomical and A. Anatomic distribution. The parts of the body (limbs, trunk, bulbar
neuro-imaging region, etc) affected by motor impairments or limitations.
findings B. Neuro-imaging findings. The neuro-anatomic findings on CT or
MRI imaging, such as ventricular enlargement, white matter loss or
brain anomaly.
Causation and Whether there is a clear identified cause, as is usually the case with
timing. post-natal CP (e.g. meningitis, head injury) or when brain
malformations are present, and the presumed time frame during which
the injury occurred, if known.
From Rosenbaum, 2007.

A classification proposed by ECDCP lists the data resulting from a report on the
definition and classification of CP in April 2006 [1, 11]. The ECDCP group indicates four
components for CP classification and maintain that all classification documentations should
include the age of the patient, from where the clinical documentation has been taken, and
what laboratory investigations have been performed.
The four components of CP are distinguished in:
1) Motor abnormalities: a) Nature and typology of the motor disorder: the type of motor
abnormalities should be related to the etiological event. The tone or movement
abnormality (e.g. hypertonia or hypotonia) should be reported and movement
anomalies reported such as spasticity, dystonia, choreoathetosis, or ataxia and
classified according to the dominant type of abnormalities while the additional tone
abnormalities should be listed as secondary type; b) Functional motor abilities.
Evaluation of upper and lower extremities should be differentiated using objective
functional scales. The committee suggests evaluating the function of the upper and
lower extremities separately using different scales. The Gross Motor Function
Classification System (GMFCS) and, specifically for the upper limbs, the Bimanual
Fine Motor Function (BFMF) have been indicated by the committee. A newer
method, the Manual Ability Classification System (MACS) for assessing arm and
hand function has also been proposed. The committee advised carrying out research
for the development of scales also for bulbar and oromotor problems and scales for
speech and pharyngeal dysfunction. In fact, as the committee referred, the
impairment of these important functions clearly resulted in daily life limitations for
the affected patients.
2) Accompanying impairments. As frequently reported, patients with CP present many
other accompanying impairments that result in severe limitations in their activities.
Seizure disorders, hearing and visual problems, cognitive and attention deficit
hyperactivity disorder, emotional and behavioral issues, and late-developing
musculoskeletal problems are frequently reported in CP patients. The presence or
absence of these dysfunctions should be recorded in the analysis of the patients
together with the course of these symptoms and the possible improvement reported.
3) Anatomic and neuro-imaging findings: a) the pattern and extent of the motor disorder
in CP with respect to different anatomical areas should be specified, including trunk,
each limb, and oropharynx, describing their involvement individually in terms of any
impairment of movements or posture. It is also recommended to avoid the terms
diplegia and quadriplegia and the examiner is invited to use the differentiation of the
unilateral versus bilateral motor involvement. b) Neuro-imaging findings: as
suggested by the American Academy of Neurology, neuroimaging-findings should
be performed on any child with CP, whenever feasible;
4) Causation and timing. Timing of insults should be indicated when there is clear
evidence, indicating the causative agent or a major component of the cause, which
was operative in a specific time-window.

Table 4. International Classification of Functioning, Disability and Health
Disability: dysfunction at 1 or more of 3 levels: impairment of body structures (organs or limbs) or

functions (physiologic or psychological), limitation in activities (execution of tasks or actions) and
restriction of participation (involvement in situation).
Classification of impairments
Motor abnormalities Hypertonic
Spasticity
Dystonia
Hyperkinetic
Chorea
Choreiform movements
Athetosis
dyskinetic
Negative motor signs
Weakness
Poor selective motor control
Ataxia
Apraxia/developmental dyspraxia
Topography or limb distribution Unilateral or bilateral involvement with indication of
upper and lower extremity function.
Classification of activity
Limitation Gross Motor Function Classification System
(GMFCS).
Functional Mobility Scale (FMS).
Manual ability classification system (MACS).
From World Health Organization, Geneva 2001.
In 2001, the World Health Organization published the International Classification of

Functioning, Disability and Health (ICF) [12]. The ICF (table 4) describes disability as
dysfunction at 1 or more of 3 levels: A) impairment of body structures (organs or limbs) or
function (physiologic or psychological); B) limitation in activities (execution of tasks or
action by the individual) and C) restriction or participation recorded as involvement in life
situations and based on the data regarding nine domains including self-care, interpersonal
relationship, schooling, and employment. Researchers frequently design studies addressing
these various domains of disability.
In 2007 an international Workshop on Definition and Classification of CP was published
by the Task Force on childhood Motor Disorders [13]
Classification of Impairment
A). Motor abnormalities. According to this classification when more than 1 type of
movement disorder is involved there is the recommendation to classify the patients
by the predominant disorder for epidemiologic purposes and listing of secondary
disorders as well. Secondary movement should be noted because this may impact
treatment decisions. The definition of motor disorders refers to the classifications of
Sanger et al. [7, 8], including hypertonic and hyperkinetic movement disorders and
negative motor signs.

1. Hypertonia is a result of spasticity, dystonia, or rigidity, the last is rarely

observed in children. A) Spasticity is reported as a component of upper motor
neuron syndrome and is associated with hyperreflexia, clonus, reflex overflow,
positive Babinski sign and weakness of pyramidal distribution. B) Dystonic
hypertonia may be associated with simultaneous agonist and antagonist
contraction. Dystonia is linked to impairment of basal ganglia and is not
associated with hyperreflexia and often disappears when the child is asleep.
2. Hyperkinetic movements are referred to as extrapyramidal symptoms and
manifest with chorea, choreiform movements, athetosis. These anomalous
movements are defined as any unwanted excess movements that are performed
voluntarily or involuntarily by the patients.
3. Negative signs. Negative signs include decreased or insufficient movements and
manifest with weakness, poor selective motor control, ataxia and apraxia/
developmental dyspraxia.
4. Topography of limb distribution. A simpler classification is advised using
unilateral or bilateral with indication of upper and lower extremity function.
B). Classification of activity limitation. Gross Motor Function Classification System.
a) The workshop group advised the use of the Gross Motor Function Classification
System (GMFCS) and the more modern scale of GMFCS-Expanded and Revised
(GMFCS-ER).
b) Functional Mobility Scale. For this function the workshop group advised the use
of the Functional Mobility Scale (FMS) as a measure of ambulatory performance
in children with CP, and the Manual Ability Classification System (MACS)
which is used to classify upper extremity performance in activities of daily living
in children with CP:
According to Moreno-De Luca et al. [3], CP can be classified based on four major
components: type and severity of the motor abnormalities, anatomical distribution, associated
impairments, and timing of the presumed causal event (prenatal, perinatal, or postnatal). A
thorough physical and neurological examination allows the identification of abnormal
neuromuscular tone (hypotonia or hypertonia) as well as the predominant type of motor
impairment, which can be spastic, ataxic, dyskinetic (dystonia or choreoathetosis), or mixed.
The characteristics and severity of the motor manifestations should be described for each limb
and the trunk, thus differentiating unilateral from bilateral involvement and establishing an
anatomical distribution (monoplegia, diplegia, triplegia, hemiplegia, and tetraplegia). These
classification systems, based on motor type and topography, are often used to infer which area
of the brain could be affected (pyramidal or extrapyramidal systems); however, they have
poor reliability even among experienced clinicians (Table 5).
Table 5. Classification based on four major components
Type and severity of the motor abnormalities

Anatomical distribution
Associated impairments
Timing of the presumed causal event (pre-, peri-, post-natal)
From Moreno-De Luca et al., 2012.

7.5. SCALES AND CLASSIFICATION FOR MOTOR ABILITIES AND

FUNCTIONAL LIMITATIONS
Motor involvement and its classic differentiation in spastic, dyskinetic, ataxic and mixed,
and related forms, attention has been moved to develop a classification regarding gross motor
function, to evaluate bimanual fine motor activity and the ability of patients with CP in using
their hands in routine situations. A scale has been prepared and used for evaluation of
communication, mode of walking and dystonic impairment.
Gross Motor Function Classification System (GMFCS). This Scale has been proposed
with the aim of following the natural course of children’s motor development with different
steps for patients affected by CP. More recently the scale has been expanded and the age of
the patients examined has been shifted up to 18 years and gross motor function rated
according to the typical performance of the CP patients rather than their best capability. The
Gross Motor Function Classification System-Expanded and Revised (GMFCS-ER) [14, 15] is
based on the use of mobility aids and performance in sitting, standing and walking activities
(Table 6). It classifies gross motor on a 5-point ordinal scale, with description of skills
provided for 5 age groups: less than 2 years of age, 2 to 4 years of age, 4 to 6 years of age, 6
to 12 years of age, and finally 12 to 18 years of age. In general the levels are as follows:
 Level I: walks without limitations

 Level II: walks with limitations
 Level III: walks using a hand-held mobility device
 Level IV: self-mobility with limitations; may use powered mobility
 Level V: transported in a manual wheelchair
Table 6. GMFCS levels I and II for children with CP
GMFCS Level I Before 2nd birthday Move in/out of sitting, floor sit with hands free to
manipulate objects, 4-point crawl, pull to stand and
cruise furniture, walk independently by 18 to 24
months.
From age 2 to 4th Move in/out of sitting and standing, walk as
birthday preferred method of mobility.
From age 4 to 6th Walk indoors and outdoors, climb stairs, emerging
birthday running/jumping.
From age 6 to 12th Walk and climb stairs without limitation, able to
birthday run and jump but speed, balance and coordination
are reduced.
GMFCS Level II Before 2nd birthday Floor sit but may use hands for support, commando
crawl or 4-point, may pull to stand and cruise.
From age 2 to 4th Move in/out of sitting, floor sit with hands free, pull
birthday to stand, 4-point crawl, cruise furniture, walk with
assistive device as preferred method of mobility.
From age 4 to 6th Sit in a chair with hands free to manipulate objects,
birthday move in/out of sitting and standing but may need

support, walk short distances indoors and on level

ground outdoors without assistive device, climb
stairs holding rail, not able to run/jump.
From age 6 to 12th Walk indoors/outdoors with difficulty on uneven
birthday surfaces or in crowds, at best minimal ability to
run/jumps.
Distinction between levels I and II
Compared with children in level I, children in level II have limitations in the ease of performing
movement transitions; walking outdoors and in the community; the need for assistive mobility
devices when beginning to walk; quality of movement; and the ability to perform gross motor skills
such as running and jumping.
From Palisano et al., 2008.
This system has been well recognized because it allows clinicians to compare the clinical
situation of the patients to that of the patients at the same age and GMFCS level with
prognostic information on the gross motor progress over time; the age of the best performance
of the gross motor function reached by the patients for each level; to evaluate the performance
of CP patients during the adolescence. This system is worthwhile in giving patients and their
families a prognosis for gross motor progress over time; and it is useful for orthopedics to
have data from wide and uniform case studies.
Functional Mobility Scale (FMS) is a system which assesses the ambulatory capacity in
children with CP [16]. The FMS is based on an interview with the parents to assess the
assistance needed for a child in covering 3 distances (5, 50, and 500 yards or meters). The
distances are not specifically expresses but represent the usual ambulation performed by CP
children at home, school, and in the community. Ratings are given for each distance category
regarding use of: 1 wheelchair; 2 walker or frame; 3 crutches; 4 sticks (canes); 5 is
independent on level surfaces; and 6 is independent on all surfaces. Rating of C (= crawling)
is assessed for the child who crawls for mobility at home (5 m) and R (does not apply) for
children who do not reach the distance (500 m) [14, 16].
Table 7. The Bimanual Fine Motor Function (BFMF)
LEVEL FUNCTION
I One hand; manipulates without restrictions.
The other hand: manipulates without restrictions or limitations.
IIa One hand: manipulates without restriction.
The other hand: only ability to grasp or hold.
IIb Both hands; limitations in more advanced fine motor skills.
IIIa One hand: manipulates without restrictions.
The other hand has no functional ability.
IIIb One hand: limitations in more advanced fine motor skills.
The other hand: only able to grasp or worse.
IVa Both hands: only able to grasp.
IVb One hand: only able to grasp.
The other hand: only able to hold or worse.
V Both hands: only able to hold or worse.
Beckung E et al., 2002.

Bimanual Fine Motor Function (BFMF) (Table 7) is applied as a complement to the

GMFCS and has been proposed to assess upper extremity function in CP. This system has
been developed for the evaluation of hand function by severity in children with CP. Various
studies have revealed that a lack of development in hand function causes a decline in sensory
information input, voluntary play, experience and learning ability, leading to a function
decline in daily life and social participation restrictions [17].
Manual Ability Classification System (MACS) (Table 8) was designed to evaluate the
ability of children with CP to use upper-extremity performance in routine activities. It
assesses performance of upper-limb tasks regardless of how they are involved, and assesses
the use of both hands together (bimanual tasks) [18]. A five categories scale is designed from
1 to 5 including: Level 1: Handles objects easily and successfully; Level II: Handles most
objects but with somewhat reduced quality or speed of achievement; Level III: Handles
objects with difficulty; needs help to prepare or modify activities: Level IV: Handles a limited
selection of easily managed objects in adapted situations: Level V:;Does not handle objects
and has severely limited ability to perform even simple actions.
For children with bilateral CP, MACS and BFMF could probably be used
interchangeably, while for children with unilateral CP, MACS provides more information
about manual abilities.
Communication Function Classification System (CFCS) is a recently proposed 5-level

classification system with the aim of helping parents and clinicians to understand how
environments influence the level of communication, and how to help in communication
assistance [19] (Table 9).
Table 8. Manual Ability Classification System (MACS)
LEVEL FUNCTION
I Handles objects easily and successfully.
II Handles most objects but with somewhat reduced quality or speed of achievement.
III Handles objects with difficulty; needs help to prepare or modify activities.
IV Handles a limited selection of easily managed objects in adapted situations.
V Does not handle objects and has severely limited ability to perform even simple
actions.
From Eliasson et al., 2006.
Table 9. Communication Function Classification System (CFCS)
LEVEL FUNCTION
I Sends and receives with familiar and unfamiliar partners effectively and efficiently.
II Sends and receives with familiar and unfamiliar partners but may need extra time.
III Sends and receives with familiar partners effectively, but not with unfamiliar
partners.
IV Inconsistently sends and/or receives even with familiar partners.
V Seldom effectively sends and receives, even with familiar partners.
From Hidecker et al., 2011.

Table 10. Barry-Albright Dystonia Scale
Lower
Eyes Mouth Neck Trunk Upper extremities
extremities
0- Absent
1- Slight dystonia less than dystonia less than pulling less than pulling less than dystonia less than dystonia less than
10% of the time and 10% of the time 10% of the time 10% of the time 10% of the time and 10% of the time
does not interfere and does not and does not and does not does not interfere and does not
with tracking interfere with interfere with interfere with with normal interfere with
speech and/or lying, sitting, lying, sitting, positioning and/or normal
feeding standing and/or standing and/or functional activities positioning and/or
walking walking functional
activities
2- Mild frequent blinking dystonia less than pulling less than pulling less than dystonia less than dystonia less than
without prolonged 50% of the time 50% of the time 50% of the time 50% of the time and 50% of the time
spasms of eyelid and does not and does not and does not does not interfere and does not
closure, and/or eye interfere with interfere with interfere with with normal interfere with
movements less than speech and/or lying, sitting, lying, sitting, positioning and/or normal
50% of the time feeding standing and/or standing and/or functional activities positioning and/or
walking walking functional
activities
3- Moderate prolonged spasms of dystonia more : pulling more pulling more than dystonia more than dystonia more
eyelid closure, but than 50% of the than 50% of the 50% of the time 50% of the time than 50% of the
eyes open most of time and/or time and/or and/or dystonia and/or dystonia that time and/or
the time, dystonia that dystonia that that interferes with interferes with dystonia that
and/or eye interferes with interferes with lying, sitting, with normal interferes with
movements more speech and/or lying, sitting, standing and/or positioning and/or with normal
than 50% of the time feeding standing and/or walking upper extremity positioning and/or
that interfere with walking function lower extremity
tracking, but able to weight bearing
resume tracking and/or function

Table 10. (Continued)
Lower
Eyes Mouth Neck Trunk Upper extremities
extremities
4- Severe Prolonged spasms of dystonia more pulling more than standard dystonia more than dystonia more
eyelid closure, with than 50% of the 50% of the time wheelchair (e.g. 50% of the time than 50% of the
eyelids closed at time and/or and dystonia that requires adapted and/or dystonia that time and/or
least 30% of the dystonia that prevents sitting in seating system), prevents normal dystonia that
time, and/or eye prevents speech a standard standing and/or positioning and/or prevents normal
movements more and/or feeding wheelchair (e.g. walking - Unable upper extremity positioning and/or
than 50% of the time - Unable to assess requires special to assess trunk function (e.g. arms lower extremity
that prevent tracking mouth head rest), movements restrained to prevent weight bearing
- Unable to assess movements standing and/or injury) and/or function
eye movements walking - Unable - Unable to assess - Unable to assess
to assess neck upper extremity lower extremity
movements movements movements
From Barry et al., 1999.

Classifications of gait analysis were constructed using a nominal scale in eight studies,
an ordinal scale in nine studies and a ratio scale in one study. The median number of
classification groups was 5 and ranged from 2 to 10. Four studies incorporated four
anatomical levels (ankle, knee, hip and pelvis) into the classification, five studies
incorporated three anatomical levels (ankle, knee and hip), four studies were based on two
anatomical levels (ankle and knee) and a further four studies were based on only one
anatomical level. In one study, the number of anatomical levels was not applicable as the
classification was constructed using stride length and cadence.
A gait pattern distinguishes: Group I: drop foot in the swing phase; Group II: tight heel
cord in the stance phase as well as a drop foot in the swing phase; Group III: more proximal
involvement (that is, restricted motion of the knee) as well as an equinus deformity of the
ankle; and Group IV: in addition restricted motion of the hip.
Barry-Albright Dystonia scale (BAD) [20], is a 5-point ordinal severity scale for
secondary dystonia and more recently the Hypertonia Assessment Tool-Discriminant (HAT)
has been developed to identify pediatric hypertonia subtypes. This system appears to be valid
and reliable for identifying spasticity and the absence of rigidity, and moderate findings for
dystonia. Every region has a severity score based only on dystonia as evidenced by abnormal
movements or postures (Table 10).
REFERENCES
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insights into the causes and classification of [corrected] cerebral palsies. Lancet
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[3] MacLennan, A. (1999). A template for defining a causal relation between acute
intrapartum events and cerebral palsy: international consensus statement. BMJ.
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[4] Cowan, F., Rutherford, M., Groenendaal, F., Eken, P., Mercuri, E., Bydder, G. M.,
Meiners, L. C., Dubowitz, L. M. S. & de Vries, L. S. (2003). Origin and timing of brain
lesions in term infants with neonatal encephalopathy. The Lancet., 361(9359), 736-742.
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perspective. Dev. Med. Child. Neurol. Suppl. 109, 3-7.
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[7] Taft, L. T. (1995). Cerebral palsy. Pediatr. Rev., 16(11), 411-418.
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(2006). Taskforce on Childhood Motor Disorders. Definition and classification of
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[10] Cans, C., Dolk, H., Platt, M. J., Colver, A., Prasaukiene, A. & Krageloh-Mann, I.
(2007). Recommendations from the SCPE collaborative group for defining and
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& Jacobsson, B. (2007). A report: the definition and classification of cerebral palsy.
Dev. Med. Child. Neurol. Suppl. 109, 8-14.
[12] World Health Organization (2001). International classification of functioning.
Disability and health. Geneva: World Health Organization.
[13] Rethlefsen, S. A., Ryan, D. D. & Kay, R. M. (2010). Classification systems in cerebral
palsy. Orthop. Clin. North. Am., 41(4), 457-67.
[14] Palisano, R., Rosenbaum, P., Walkter, S. et al., (1997). Development and reliability of a
system to classify gross motor function in children with cerebral palsy. Dev. Med.
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[15] Palisano, R., Rosenbaum, P., Bartlett, D. & Livingston, M. (2008). Content validity of
the expanded and revised Gross Motor Function Classification System. Dev. Med.
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[16] Graham, H. K., Harvey, A., Rodda, J., Nattrass, G. R. & Pirpiris, M. (2004). The
Functional Mobility Scale (FMS). J. Pediatr. Orthop. 24(5), 514-20.
[17] Beckung, E. & Hagberg, G. (2002). Neuroimpairments, activity limitations, and
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Classiﬁcations of cerebral palsy

Chapter · January 2015

Vito Pavone Gianluca Testa

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CLASSIFICATIONS OF CEREBRAL PALSY

Vito Pavone* and Gianluca Testa

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Keywords: cerebral palsy, CP classification, Gross Motor Function Classification System,

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Figure 2. Hyperextension of lower limbs following suspension maneuver

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Figure 5. Scissoring feature of lower limbs.

Figure 6. Spastic quadriplegia with sever involvement of the upper limbs.

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Figure 8. Severe brain suffering with extensive cystic areas.

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Figure 9. Periventricular brain cyst secondary to hypoxic-ischemic injury.

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7.4. PREVIOUS CLASSIFICATIONS

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Table 1. Clinical classification of CP based on clinical description [7]

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Table 2. SCPE Classification of CP

Spastic CP Increased tone and abnormal reflexes.

The application of the system advised by SCPE with application of inclusion/

Table 3. Components of CP classification (ECDCP)

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Table 4. International Classification of Functioning, Disability and Health

Disability: dysfunction at 1 or more of 3 levels: impairment of body structures (organs or limbs) or

In 2001, the World Health Organization published the International Classification of

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1. Hypertonia is a result of spasticity, dystonia, or rigidity, the last is rarely

Table 5. Classification based on four major components

Type and severity of the motor abnormalities

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7.5. SCALES AND CLASSIFICATION FOR MOTOR ABILITIES AND

 Level I: walks without limitations

Table 6. GMFCS levels I and II for children with CP

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support, walk short distances indoors and on level

Table 7. The Bimanual Fine Motor Function (BFMF)

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Bimanual Fine Motor Function (BFMF) (Table 7) is applied as a complement to the

Communication Function Classification System (CFCS) is a recently proposed 5-level

Table 8. Manual Ability Classification System (MACS)

Table 9. Communication Function Classification System (CFCS)

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From Barry et al., 1999.

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