The Definition of 

Cerebral Palsy
2
Eve Blair and Christine Cans

Abstract
Cerebral palsy (CP) should not be considered as a diagnosis but as a label;
it is an umbrella term. The definition is not sufficiently precise to guaran-
tee agreement as to which patients to include under this label, but the addi-
tional inclusion criteria required are not yet internationally standardised.

2.1 Definitions
Cerebral palsy (CP) is the term applied to a
group of children with motor impairment and
related service requirements. Since this group is
heterogeneous with respect to clinical signs, aeti-
ology and pathology, it has frequently been sug-
gested that it is more appropriate to refer to the
cerebral palsies, in the plural.
The word palsy undoubtedly has its roots in
ancient Greek. It is most likely derived from
paresis (πάρεση in Greek) denoting weakness
[1]. However the term ‘cerebral palsies’ was
probably not coined until the late 1880s by
William Osler, a Canadian physician (see also
E. Blair
Telethon Kids Institute,
University of Western Australia, Perth, WA, Australia
e-mail: Eve.Blair@telethonkids.org.au
C. Cans (*)
Universite Joseph Fourier Grenoble,
Grenoble, France
e-mail: christine.cans@gmail.com
Chap. 1) [2, 3]. Between 1950 and 2000, several
authors published rather similar definitions of
CP [4–8]. The Mutch et al. [7] paper, commis-
sioned by the UK Spastic Society, was the result
of several meetings held in Europe and America.
On account of the well-recognised heterogeneity
seen in CP, it was agreed at these meetings that it
did not refer to a unique disorder but that it was
nonetheless a useful umbrella term. A European
consortium of professionals involved in the CP
field were responsible for the SCPE [8] paper
in which we read: ‘Cerebral Palsy is a group
of permanent, but not unchanging, disorders of
movement and/or posture and of motor function,
which are due to a non-progressive interference,
lesion, or abnormality of the developing/imma-
ture brain’.
At a 2004 workshop held in Washington, the
utility of retaining the term CP was discussed
at length since the label does not inform aeti-
ology, severity or even prognosis, given that
should the cerebral pathology progress, it is the
label that is retrospectively removed. However
it was agreed to retain the term since in an age
of electronic databases, it is a conveniently

© Springer International Publishing AG 2018 13

C.P. Panteliadis (ed.), Cerebral Palsy, https://doi.org/10.1007/978-3-319-67858-0_2
14
unique, w ­ ell-­recognised and understood search
term. Following this workshop, Rosenbaum
et al. [9] published the following: ‘Cerebral
palsy describes a group of permanent disorders
of the development of movement and posture,
causing activity limitation, that are attributed to
non-­progressive disturbances that occurred in the
developing fetal or infant brain. The motor disor-
ders of cerebral palsy are often accompanied by
disturbances of sensation, perception, cognition,
communication, and behavior, by epilepsy, and
by secondary musculoskeletal problems’. This
definition is followed by an annotation concern-
ing the terms used and was accompanied by sev-
eral commentaries (e.g. [10]).
The differences between the SCPE [8] and
Rosenbaum [9] definitions lie primarily in the
choice of words: motor function is replaced by
‘activity limitation’ and ‘developing/immature
brain’ by developing fetal or infant brain. The
latter definition also expresses the possibility that
additional impairments coexist, a fact that was
neither excluded by earlier definitions nor neces-
sary for acquiring the CP label.
All definitions have four elements in common:
(1) disorders of movement or posture leading to
motor impairment that (2) develop very early in
life (3) can be attributed to cerebral abnormality,
and (4) although the clinical signs change with
the child’s development, the cerebral abnormality
neither resolves nor deteriorates.
These four elements make it clear that CP is a
man-made construct defined by clinical descrip-
tion rather than by any objective biological, aeti-
ological or anatomic criteria; other than that the
primary responsible pathology is sited in the
brain and not in other elements contributing to
motor function such as the spinal cord or mus-
cles. Thus CP should not be considered a diagno-
sis but as a useful label to group patients likely to
benefit from related management strategies, an
umbrella term for many different pathological
and aetiological diagnoses, not all of which are
yet recognised but middle cerebral arteria infarc-
tus, CMV maternofetal infection, periventricular
leukomalacia due to very preterm birth, lissen-
cephaly, cardiovascular accident and kernicterus
represent some examples.
E. Blair and C. Cans
Although these definitions for CP are useful,
they are not sufficiently precise to guarantee
agreement as to which individuals to include
under the label. Observers of CP have therefore
had to formulate their own sufficiently precise
inclusion criteria, which has resulted in there
being variations between them.
2.2 Elements Varying Between
Sets of Inclusion Criteria
for CP
Consensus with Freud’s phenomenological
approach that CP is defined exclusively by clini-
cal description [11] is gaining greater acceptance
[8, 12]. However this was not always the case.
In the past CP was often considered a ‘diagno-
sis of exclusion’. If aetiology was known, then
it was argued, the individual could not also be
‘diagnosed’ as CP. This led to the exclusion
of the most easily recognised aetiologies (e.g.
those with a genetic cause or known syndrome
or with chromosomal anomaly), even when the
clinical criteria for inclusion were met [13].
With this approach, increasing diagnostic power
would decrease the reported prevalence of those
labelled CP even in the absence of any change
in prevalence of symptoms. However, for long-
term registers that had continued to exclude
historically excluded diagnoses, embracing the
phenomenological approach in its entirety risked
artificially increasing apparent prevalence in their
estimation of time trends, leading to the publica-
tion of ‘What constitutes CP?’ [14] which tried
to define which diagnoses were and were not
included. With the recognition that the propor-
tion of CP with such historically excluded diag-
noses was very small and the increasing number
of new registers for whom this was not an issue,
the subsequent ‘What constitutes CP?’ paper [12]
fully embraced the phenomenological approach.
There are a number of characteristics to be
considered when deciding whether to include a
person under the CP umbrella, and algorithms
have been found useful to increase reliability of
labelling [8, 12], but controversy remains con-
cerning a few issues.
2  The Definition of Cerebral Palsy
2.2.1 T
 ype of Disorder of Movement
or Posture
Spasticity, dyskinesia and ataxia are always
included but the rarely encountered isolated
hypotonia is excluded by European but included
by many Australian and US workers, though fre-
quently with caveats. In Western Australia iso-
lated hypotonia is only included if not attributable
to cognitive deficits and contributes only 1% of
congenital CP [15].
2.2.2 S
 everity of Disorder
of Movement or Posture
In the past, the severity of CP has been considered
to be that of the primary motor impairment (e.g.
the degree of spasticity or dystonia) but is now
usually assessed from motor functional ability. Of
24 CP surveillance programmes surveyed, only 9
included a criterion purporting to address mini-
mum severity in their definitions of CP [16]. Four
programmes required activity limitation clarified
as ‘difficulties an individual may have in execut-
ing activities’ [9] with only one stipulating that the
limitation must be due to motor impairment. Since
the activities are not defined and everyone has dif-
ficulty, for want of strength, flexibility or prac-
tice, in executing some activities that others may
accomplish with ease, it remains a subjective cri-
terion for severity, the necessity of motor impair-
ment making it somewhat more objective. Five
further programmes require a minimum Gross
Motor Function Classification System (GMFCS)
level of I [17] despite it reflecting only lower
limb function. GMFCS level I children can run
and jump in late childhood but with suboptimal
speed, balance and coordination, the same activ-
ity limitations observed in the clumsy child, yet
it is generally agreed that ‘merely’ clumsy chil-
dren are excluded. One further population based
register specifies that abnormal neurological signs
are required but that functional impairment is not
required to be described as minimal CP.
Defining the boundary of the milder end of the
CP spectrum remains problematical, particularly
15
since in some jurisdictions, the CP label may be
allocated in order to gain access to medical ser-
vices such as botulinum toxin.
2.2.3 H
 ow Early in Life Can
the Disorder of Movement or
Posture Be Reliably
Recognised?
The earlier that CP can be recognised, the better
in terms of providing optimal care for the child,
informing parents and maximising the informa-
tion that can be retrieved for epidemiological
purposes. Signs of disordered motor control may
be present very soon after birth, and satisfactory
prediction of CP from abnormal general move-
ments has been demonstrated by 20 weeks post-­
term age by trained observers in high-risk infants
either born very preterm or with neonatal neuro-
logical signs (e.g. [18–20]). These high-risk
infants contribute almost half of congenital CP,
and the increasing availability of trained observ-
ers allows the ‘at high risk of CP’ label to be
assigned before, even well before, 5 months post-­
term age. However, the motor disorders that
define CP neither resolve nor deteriorate and are
generally considered to refer to voluntary move-
ment and posture. Since verification of these
characteristics must await development, 10 of 24
surveillance programmes include only children
who survive to a specified minimum age which
varies between 1 and 16 years [16]. However
excluding early deaths risks excluding the most
severe end of the CP disability spectrum, chil-
dren who would uncontroversially have exhib-
ited severe CP had survived. If severity of
impairment correlates with severity of the causal
factors, this would exclude those in whom causal
factors may be most easily recognised and is the
reason that a narrow majority of surveillance pro-
grammes do not define a minimum age of sur-
vival but accept any definite description of CP by
‘a suitably qualified person’. It is not clear if or
when observers trained in recognising abnormal
general movements will be considered ‘suitably
qualified persons’.
16 E. Blair and C. Cans

2.2.4 P
 rogression or Resolution relevant cerebral pathology believed to be
of the Cerebral Abnormality acquired before 28 days of life is usually, though
not always particularly in developing countries,
All definitions make it clear that to meet criteria grouped together. Even in developed countries,
for the CP label, the cerebral pathology neither there are exceptions such as term or near-term
resolves nor progresses. Should this occur in a infants who suffer traumatic accidents days or
child labelled as CP, the CP label is removed as weeks after being discharged from the birthing
the defining criteria are no longer met. So, location as neurologically intact. Such an infant
although the initial categorisation as CP is based may be included with infants meeting the criteria
on neurological examination, the continued for CP after acquiring brain damage postneona-
appropriateness of that label is not assured. With tally. These have been reported to contribute
increased diagnostic capabilities, aetiological between 4.6% and up to 60% of all CP in devel-
diagnoses for children with the CP label are now oping countries, the proportion correlating with
identified more frequently, and it may be possible social disadvantage [22]. The upper age limit of
to exclude a child from the CP category on the acquisition of cerebral damage, after which any
grounds of having an aetiological diagnosis that resulting impairment is not included as CP, varies
is known to be progressive, even before that pro- between 2 and 10 years, with 2 and 5 years being
gression becomes apparent, for example, with the most popular choices [16]. However since
genetically diagnosed Rett syndrome [21]. Such most postneonatally acquired CP is acquired by
diagnoses apply only to the minority, so to 2 years of age [15], variations in upper age limit
increase the objectivity of this criterion, most have little effect on estimations of prevalence.
registers define a cut-off age (typically the age of Despite extensive research, the causal path-
ascertainment) by which resolution or progres- ways to CP are not well understood, at least in
sion must be identified if a potential registrant is part because there are so many such causal paths,
to be excluded. each responsible for only a small proportion of
An associated conundrum is the differentia- all CPs. However the majority of the more than
tion between degeneration and repeated insults. 800 CP-related research papers published annu-
Some vascular or metabolic defects create a vul- ally are devoted to the management of CP. This
nerability to brain damage which may occur once plethora of literature, sometimes with conflicting
or repeatedly depending on environmental cir- conclusions, complicates the work of the physi-
cumstances, including treatment. Smithers-­ cian and is the reason for this book. The spectrum
Sheedy et al. propose that such conditions be of CP management has many factors that demand
included since they are not inherently progressive new and up-to-date knowledge by a group of
despite the possibility that they may appear pro- experienced doctors, nurses, physiotherapists and
gressive and, in the absence of the diagnosis others that work with individuals with CP in
being recognised, may well have been excluded order to achieve the best possible outcomes.
[12].

References
2.2.5 H
 ow Early in Life Must
the Cerebral Abnormality
Be Acquired?
It is agreed that cerebral pathology acquired pre-
natally and intrapartum is included. Since the
precise timing of perinatally acquired brain dam-
age may be difficult to identify and often has its
origins in the prenatal or intrapartum periods, all
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