SPECIAL ARTICLE

A CLASSIFICATION OF CEREBRAL PALSY

By W. L. Minear, M.D., Ph.D.

A REvuw of the literature reveals con- which the olden term, cerebral spastic paral-
fusion in nomenclature and classifica- ysis, is only one of the group. It is fre-
tion in the field of cerebral palsy. Using as quently a combination of both motor and
a basis the majority opinion from question- sensory involvement. It was formerly con-
names sent to the members of the American sidered as involving only a motor handicap,
Academy for Cerebral Palsy during 1953 and on this basis confusion arose among
(all members were polled; 64 per cent re- those treating such cases, since the other
plied) by the Nomenclature and Classifica- associated handicaps were not recognized
tion Committee, the following classification and difficulties arising from treating these
for cerebral palsy is presented. children were attributed to their being
A complete diagnosis should include one mentally defective. However, it is very diffi-
on more titles from each of the main head- cult to explain how mental deficiency can
ings of this nomenclature. The motor classi- be associated with pure athetosis on ataxia.
fication is given precedence. Next, there The brain is a very complicated organ and
should be a statement as to topography of any injury or lack of development in it gives
the disease (body pants involved). There rise to unusual disturbances of function,
also should be a statement as to the etiology both along the line of motor control and
of the disease. A statement of the capabili- sensation. This places cerebral palsy in a
ties of the patient should include the pen- group by itself, being made up of more than
tinent motor, sensory, intellectual, emo- one entity depending on the area injured,
tional, visual, speech, and hearing status, diseased, or defective.” (From lecture notes
and should be made under each heading of Winthrop Phelps.)
in the supplemental classification. If the In Cerebral Palsy: Its Individual and
pathology in the brain has been determined Community Problems by Denhoff, as a
accurately at necropsy or by means of standard definition, reference is made to
electroencephalograms, pneumoencephalo- Perlstcin who is quoted as stating that cere-
grams, or surgical exploration, a statement bral palsy is generally defined as a “condi-
of structural disease should be made (neu- lion, characterized by paralysis, weakness,
roanatomical diagnosis). Finally, a state- incoordination, or any other aberration of
ment of the functional and therapeutic motor function due to pathology of the
classification of the patient completes the motor control centers of the brain.” A limited
list. Thus, a comprehensive diagnosis will definition cited by Denhoff is one wherein it
demand a careful consideration of every is conceived as “a condition in which inter-
aspect of the patient and will afford a fenences with the control of the motor sys-
sound basis for prognosis, neuroanatomical tem arises as a result of lesions occurring
correlation, and treatment. from birth trauma.” The practical definition,
according to Dcnhoff, warrants serious con-
CEREBRAL PALSY DEFINED sideration : “One component of a broader
“The term, cerebral palsy, constitutes five brain damage syndrome comprised of neu-
main classes of handicapped children, of romotor dysfunction, psychological dys-

Dr. Minear is Chairman, Nomenclature and Classification Committee, American Academy for Cere-
bra! Palsy. The proposed classification has the approval of the American Academy for Cerebral Palsy.
This classification has been reviewed by the Committee on the Handicapped Child of the American
Academy of Pediatrics and receives the endorsement of this committee.

841

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842 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

function, convulsions, and behavior dis- disturbances should be excluded as well as

orders of organic origin. those primarily the result of spinal cord
“The characteristics of the cerebral pal- lesions.”
sied child are paralysis, weakness, inco- Cruickshank and Raus,6 state : “As a dis-
ordination, on any other aberration of motor ease, cerebral palsy is not progressive nor
function due to malfunction of the motor is it contagious or epidemic in form. As a
centers of the brain. neuro-physical and neuro-psychological
“He may also have other symptoms which deviation, however, it is basically a disease.
reflect a damaged brain. There may be con- Glidden Brooks has correctly spoken of
vulsions, mental retardation on deficiency, cerebral palsy as a ‘long-term, non-fatal,
vision, hearing or perceptual problems, as non-curable disease.’ He considers it a dis-
well as speech, behavioral and emotional ease in the sense of the present discussion.
disturbances. It is non-curable, but oftentimes amenable
“The underlying cause of these symp- to therapy and training. It is non-fatal per
toms-brain damage-is not a specific type. Se.
Rather similar pathological findings are Cerebral palsy comprises those motor and
found in such clinical entities as mental other symptom complexes caused by a non-
deficiency, epilepsy, amid behaviour dis- progressive brain lesion (or lesions). The
orders or organic origin. Thus originates characteristic thing about cerebral palsy is
the term ‘brain damage’ syndrome which in- that it is a well defined entity with a
eludes cerebral palsy along with other con- variety of etiologies and pathologies. When
ditions mentioned. clinical syndromes become better deline-
“Cerebral palsy is the neunomotor com- ated with respect to known etiologies and
ponent of the ‘brain damage’ syndrome. It pathological changes, they too can be re-
must always be kept in mind that the cere- moved from the general category of cere-
bral palsied child may suffer from any other bral palsy, and placed in their own cate-
component or components of the syndrome gonies. For example, it is not unlikely that
along with the neuromotor handicap. bilirubin encephalopathy will someday be
“The concept of the ‘brain damage’ syn- removed from the category of cerebral palsy
drome has many practical applications, par- and given its own name. In the aging,
ticularly from an educational and ‘parent arteriosclerosis or parkinsonian disease can
understanding’ viewpoint. It negates the cause a change in the patient who has had
propaganda that the cerebral palsied child cerebral palsy since infancy or childhood,
presents a problem unique from that of but these are morbid entities superimposed
other similarly handicapped children.” on the original lesion causing the cerebral
J ohn F. Pohl defines cerebral palsy as palsy.
follows : “Cerebral palsy is the term used to The decision of the American Academy
designate a group of neuromuscular dis- for Cerebral Palsy to delete neoplastic brain
orders in which there is impairment or loss diseases and the progressive neurological
of muscular control due to a lesion of the degenerative diseases of the brain has sev-
brain.” cral important advantages. This decision
C. L. Balf and T. T. S. Ingram, in a reduced the field of cerebral palsy to a more
recent article,2 state as follows : “Cerebral logical and manageable unit. The treat-
palsy is a descriptive term, applied to a ment of brain neoplasms is frequently sur-
group of motor disorders of young children, gical or radiological and the treatment pro-
in whom full function of one on more limbs gram depends on the type of neoplasm. It
is prevented by panesis, involuntary move- is a great mistake to treat a brain neoplasm
ment, on incoondination. Tacit agreement as cerebral palsy. Obviously, the correct
has been reached that progressive diseases diagnosis should be made and the proper
and those characterized by transient motor treatment program carried out.

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 AMERICAN ACADEMY OF PEDIATRICS - SPECIAL ARTICLE 843

After the tumor is removed and there is often sensory involvement in the areas of
no danger of recurrence, the patient may proprioception to point discrimination and
form perception. Aphasias appear more fre-
then be accepted to the ranks of those with
quently in right than in left hemiplegias and
cerebral palsy to be treated symptomati-
are much more common in the acquired than
cally for residuals of the lesion. The same in the congenital cerebral palsy.
is true for a child with hydrocephalus, D. Triplegia
traumatic on infectious damage to the brain. Involves 3 extremities, usually both legs and
one arm, usually spastic. This may represent
Under the new definition, the patient is
hemiplegia plus paraplegia, or incomplete
not accepted as cerebral palsy until a pro-
quadriplegia. In the latter case, both arms
gnessive nature of the etiology has been will be equal or nearly equal in length. In
eliminated. This does not mean that treat- the former, the involved arm will be shorter.
ment technique suitable for cerebral palsy E. Quadnplegia
(Tetraplegia) Involvement of all 4 extremities.
cannot be used on patients with progressive
Patients greatest
with involvement
the of
brain lesions, but rather that attention
the legs are usually spastic, and patients with
should be concentrated on the treatment greatest involvement of the arms are usually
and elimination of progressive damage to the dyskinetics, including athetoids.
the brain as long as this is a possibility. F. Diplegia
This term is seldom used. “Paralysis affecting
CLAssIFICATIoN OF CEREBRAL PALSY#{176} like parts on either side of the body; bilateral
paralysis.” (The American Illustrated Mcdi-
I. Physiological (motor)
cal Dictionary, Dorland, 21st Edition.)
A. Spastic C. Double Hemiplegia
B. Athetotic This term is seldom used. implies those
“. . .

Types of athetosis accept-

cases in which the arms are more involved
able to the American than the legs. These are usually spastic in
Academy for Cerebral type.” (Cerebral Palsy-Its Individual &
1 . Tension
Palsy to date. For outline
2. Non-tension
Community Problems, edited by William M.
of 12-types of athetosis Cruickshank, Ph.D. and George M. Raus,
3. Dystonic
described by Winthrop M.D., Syracuse University Press, 1955.)
4. Tremor
Phelps, see “Types of
III. Etiological
Cerebral Palsy Defined”
herein. A. Prenatal
C. Rigidity 1. Hereditary-Genetically transmitted and
D. Ataxic may involve racial or familial predilections
E. Tremor and often sex-linked. These are often
F. Atonic (rare) classified as “cerebral agenesis.” The
C. Mixed symptoms are often present at birth and
H. Unclassified generally do not progress. Examples : Her-
editary athetosis, familial tremor, familial
II. Topographical spastic paraplegia.
A. Monoplegia 2. Acquired in utero
Involves one limb; condition is rare; should a. Prenatal infection
(toxoplasmosis)
be checked closely to determine if you are rubella, or infection.
other maternal
not dealing with a paraplegia or hemiplegia. b. Prenatal anoxia-carbon monoxide, or
B. Paraplegia strangulation of mother, maternal
Involves the legs only and practically always anemia, hypotension, e.g., following
of the spastic or rigidity type. spinal anesthesia, placental infarcts, or
C. Hemiplegia placenta abruptio, kinking, knots or
The lateralized one-half of the body is af- prolapse of the cord.
fected and it is usually spastic, although pure c. Prenatal cerebral hemorrhage-ma-
athetoid hemiplegias are occasionally seen, ternal toxemia, direct trauma, ma-
as are pure rigidity hemiplegias. There is temal bleeding diathesis.
d. Rh factor, Kernicterus due to Rh factor
0 The form of the following classification, in gen- (conoversial).
era!, is patterned after that which has been sue- e. Metabolic disturbances, diabetes.
cessfully used for some years by the American f. Gonadal irradiation, harmful exposure
Heart Association. to x-ray.

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844 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

g. Maternal malnutrition. b. Field defects

B. Natal 2. Motor
1. Anoxia a. Conjugate deviations (33%) of motor de-
a. Mechanical respiratory obstruction. fects)
b. Atelectasis. b. defects
Fixation
C. Narcotism (due to drugs). C. Spasmus fixus (1%)
(1. Placenta previa or abruptio. (1. Strabismus fixus (1%)
e. Maternal anoxia or hypotension. C. Esotropia (51%)
f. Breech deliveries with delay of the f. Exotropia (9%)
after-coming head. g. Hypertropia
g. Bleeding in the first trimester (see h. Hypotropia
Eastman). i. Nystagmus
C. Postnatal j. Pseudopalsy of the exteriii (22%)
1. Trauma-Subdural hematoma, skull frac- C. Auditory status

itires, wounds and contusions of the brain 1. Pitch range loss

(accidental). 2. Decibel loss
2. Infections-(more common in children H. Speech disturbances
than adults) meningitis, encephalitis, brain
V. Neuroariatomical (See subheadings under
abscess.
“Brain,” topographic headings, Standard
3. Toxic causes-Lead, arsenic, coal tar de-
rivatives, streptomycin, etc.
Nomenclature of Diseases and Operations.)

4. Vascular accidents (more common in adults Failure to discuss the

parts of the brain involved
than children) congenital aneurysms, circle in the different motor types of cerebral palsy is de-
of Willis, hypertensive encephalopathies, liberate. This discussion is reserved until after we
emboli due to bacterial endocarditis or correlate the lesions from a sufficient number of
fat embolism, cerebrovascular thrombosis, brains from patients with cerebral palsy with the
in debilitated infants, sudden pressure symptoms to gain a scientific understanding of the
changes. problem.
5. Anoxia-Carbon monoxide poisoning, The following two headings are added for the
strangulation, high altitudes, and deep sake of completeness, and for the use of the dm1-
pressure anoxia, hypoglycemia. cian studying the cerebral palsied patient. They are
6. Neoplastic, or late development defects- not intended to be used for coding by the medical
Brain tumors, brain cysts, internal hydro- record librarian:
cephains, hydrocephalus.
VI. Functional Capacity (degree of severity)
Iv. Supplemental Class I. Patients with cerebral palsy with no
practical limitation of activity.
A. Psychological evaluation
Class II. Patients with cerebral palsy with slight
1. Degree of mental deficiency, if any.
to moderate limitation of activity.
B. Physical status
Class III. Patients with cerebral palsy with
1. Physical growth evaluation (Wetzel Grid
moderate to great limitation of activ-
or other)
ity.
2. Developmental level (Gesell)’
Class IV. Patients with cerebral palsy unable
3. Bone age
to carry on any useful physical activ-
4. Contractures
ity.
C. Convulsive seizures
D. Posture and locomotive behaviour patterns VII. Therapeutic
E. Eye-hand behavior patterns Class A. Patients with cerebral palsy not requir-
1 . Eye dominance ing treatment.
2. Eye movements Class B. Patients with cerebral palsy who need
3. Eye postures minimal bracing and minimal therapy.
4. Fixation Class C. Patients with cerebral palsy who need
5. Convergence bracing and apparatus, and the serv-
6. Prehensory approach ices of a cerebral palsy treatment team.
7. Grasp Class D. Patients with cerebral palsy limited to
8. Manipulation such a degree that they require long
9. Hand dominance term institutionalization and treatment:
F. Visual status
1. Sensory The American Academy for Cerebral
a. Amblyopia Palsy also agreed to: (1) Delete neoplastic

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 AMERICAN ACADEMY OF PEDIATRICS - SPECIAL ARTICLE 845

and progressive neurological diseases from 3) The decision of the American Academy
the cerebral palsy classification. (2) Co-op- for Cerebral Palsy to include the manifesta-
crate with the Editor of Standard Nomen- tions of nonprogressive (static) brain lesions
clature of Diseases and Operations1 to pre- as cerebral palsy was probably the most
pare a classification and coding based on important single decision. The field of cene-
the accepted classification along with the bral palsy is now clearly limited to a more
following recommendations: (a) Delete the logical and manageable size. Furthermore,
term “cerebral spastic infantile paralysis” progressive brain lesions should be classi-
and substitute “cerebral palsy.” (b) Assign fled so as to place emphasis on etiology.
code numbers for the 6 motor types of
cerebral palsy, amid a code number for SCOPE OF FUTURE CLINICAL
WORK OUTLINED
“cerebral palsy, type unknown” (Note: The
nuxed type may be coded using two on For the time being, the clinician had best
more of the type code numbers). be practical and resolve to make a careful
symptomatic analysis of patients with cere-
POINTS FAVORING THE MOTOR
bnal palsy using all clinical tools available
CLASSIFICATION AS
to him; treat the total patient symptomati-
FIRST CHOICE cally and co-operate with the Brain Regis-
The consensus giving the motor classifi- try in collecting, studying and correlating
cation first choice instead of the etiological the symptoms with lesions. This then is the
on netiroanatomical classification is as fol- primary work of the clinician : Let him use
lows: a classification that fits his purposes in a
1) The treatment is primarily the treat- practical way-Let him cOncentrate on the
ment of symptoms, not the etiology or the phase of cerebral palsy which, by training
portion of the brain involved. Etiology fne- and opportunity, he is best able to make,
quently cannot be determined, but it is then he will at least be doing his part well.
highly important to include it in the diag- It appears that we, as clinicians, are missing
nosis when it can be determined (even a lot in our clinical evaluation of the child
when determined, the treatment will be with cerebral palsy, especially in the realm
symptomatic). Since the treatment of cere- of sensory involvement. Probably this is
bnal palsy is symptomatic, a classification true because we are just beginning to work
l)ased on major presenting symptoms is use- out techniques to treat the sensory losses.
ful and practical. Moreover, if etiology is We have concentrated on the motor and
known, the eventual pathology and patho- intellectual phases of cerebral palsy and
genesis can better be studied. neglected the sensory phase. If the student
2) The neuroanatomical classification of medicine can grasp and understand the
based on position, extent, and character of clinical manifestations of cerebral palsy,
the brain lesion, is highly desirable from a he will have broadened his knowledge of
scientific point of view, but is presumptive medicine considerably.
without necropsy, although electroenceph-
alogram and air studies give important in- TYPES OF CEREBRAL PALSY DEFINED
formation. When the Brain Registry of the Cerebral palsy comprises those motor and
American Academy for Cerebral Palsy has other symptom complexes caused by a non-
studied more brains and correlates lesions progressive brain lesion (or lesions). The
with primary presenting symptoms, we will various sub-types may be defined as fol-
be able to evolve a neuroanatomical diag- lows:
nosis for cerebral palsy. Even then, the A. Spasticity-Chanactenized by a lower
diagnosis in the living will be based on threshold of the stretch reflex, an enlarged
inference and the treatment will still be the neflexogenic area, augmented responses with
treatment of symptoms. clonus, and an abnormal electromyographic

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846 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

record (synchronization of discharge rate in C. There is usually little involvement in the

various parts of the spastic muscle). The hands, fingers, wrists, or knees.
D. Arms and legs describe these flailing motions,
pathological stretch reflex must be present
usually fully extended, sometimes flexed.
to make a diagnosis of spasticity. There is E. Doctor Phelps has never seen flail(ing) athe-
a tendency toward greater involvement and toids live beyond maturity. Apparently there
contractures, affecting the antigravity mus- is some progression of the disease between
10 and 14, with gradual weakening of the
des.
muscles of breathing followed by flaccidity
B. Athetosis-Chanactenized by an ab-
and death.
normal amount and type of involuntary mo-
Note: This resembles one of the rare progressive
tion, normal reflexes, normal clcctromyo- neurological diseases and since it is progressive,
graphic findings, uncontrolled, involuntary would be excluded from the new classification. The
and inco-ordinate motions with varying de- cause of death in this type of athetosis is not known.
Doctor Phelps prefers to retain this entity for the
gnces of tension. Description of the various
sake of completeness.
clinical types by Winthrop Phelps2#{176}follows:
VI. Tension
I. Rotary
A. A state of muscular tension in an anthetoid
A. The most common type.
(rotary, tremor or dystonic) hiding the char-
B. Involves muscles which can take part of
acteristic motions of the types.
rotary motions.
B. When the tension is relieved the true nature
C. The rotary motions are usually rather slow,
of the athetosis (rotary, tremor or dystonic)
sometimes extremely slow.
is revealed.
D. The feet describe a circular motion; the hands
C. Must be
distinguished from spasticity, in
pronate and supinate; the shoulders internally
which stretcha reflex must be present and
and externally rotate.
from rigidity in which the lead-pipe-like
E. There may be varying degrees of tension.
resistance of the muscle is found.
II. Tremor (tremor-like) D. The state of tension is not constant, and can

A. Almost as common as the rotary type. be shaken out by the examiner.

B. There is an irregular and uneven type of E. The athetoid is only classed as tension athe-
involuntary contraction and relaxation which
toid when the tension is the outstanding
characteristic and masks the rotary, tremor,
involves flexor and extensor, and abductor
and adductor mechanisms.
or dystonic features.

C. Rotary motion is not seen. Involuntary rotary

VII. Non-tension
motion is not seen. The motion is not a true
tremor. A. This is also a transient state and might mask
other types of athetosis.
III. Dystonic B. In infancy it is often mistaken for the rare
A. The extremities assume distored positions atonic type of athetosis.
held involuntarily for periods of from a few C. Involuntary motion must be present.
seconds to a few minutes. D. Non-tension athetosis is frequently seen in
B. The dystonic motions may involve neck, small babies and is usually the first identifi-
trunk, arms, and legs. able symptom. As the child grows, one of the
C. An entirely different distorted position may first five types mentioned above can be identi-
be assumed within the passage of a few fled.
minutes. Note: It must be understood that both “tension”
and “non-tension” are temporary classifications of
Iv. Shudder patients under treatment.
A. Closely resembles the shudder that any
normal person may experience. VIII. HemiathetosLs

B. The shudder may be violent, causing patient A. This stricily

is a topographical classification
to fall on the floor or simply a mild shudder- and made when rotary,
is tremor-like, dy-
like motion going through the arms and legs. stonic, or shudder athetosis involve one side
of the body.
V. Flail(ing) B. Doctor Phelps has not seen a hemi-flail(ing)
A. A rare type of athetosis. athetosis.
B. Arms and legs are thrown around rather
violently from the axial shoulder and hip Ix. Neck and Arm.
joints. A. This type is limited to the head, neck, and

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 AMERICAN ACADEMY OF PEDIATRICS - SPECIAL ARTICLE 847

shoulder girdle, with little or no athetosis XII. Emotional Release

in the legs. . A. Usually the rotary or tremor-like athetosis is
B. Some of these learn to typewrite or pick tip present, combined with release of the laugh-
objects or write with their toes. ing, crying and anger mechanisms. A very
C. There may be or may not be a speech defect. slight stimulation for laughter or crying will
D. The motion may be rotary, tremor-like, dys- produce the whole picture of this emotion
tonic, or shudder, but most of them are dys- without any particular background of feel-
tonic. ing of the emotion.
E. Doctor Phelps thinks it advisable to use the B. The patient does not like the emotional dis-
separate classification of neck and arm athe- plays, but depending on the tension associ-
tosis for determining the best plan for place- ated with the athetosis present, the reaction
ment and treatment. may be more or less marked.
Note: Not all these types of athetosis have been
x. Deaf Athetosis
accepted by the Academy, but are listed for the
A. Athetosis with etiology of Rh incompatibility,
sake of completeness.
usually showing some degree of hearing loss.
B. Deafness may be slight enough so as to be C. Rigidity-A disturbance of the ago-
of no importance in speech or education. nist-antagonist relations with resistance to
C. There is often loss of high pitch or high
slow passive motion of both agonist and
frequency tones with essentially normal hear-
ing in the lower pitch ranges. They often
antagonist muscles. If the resistance to
hear low pitch sounds very well and give the passive motion is continuous, it is referred
parent and casual observer the impression to as the “lead-pipe” rigidity-if discon-
that
their hearing is keen.
tinuous, “cog-wheel” rigidity. The resist-
D. Child usually learns to become an automatic
ance is greater to slow than to rapid mo-
lip reader, especially for consonant sounds.
E. The specific pitch range lost is usually above tion, whereas, in spasticity, there is greater
2,048 or, more frequently, between 4,098 resistance to rapid motion. In rigidity, the
and above. antagonists to the antigravity muscles are
F. There may be no athetosis in the tongue, most involved. Total motion may be de-
throat and lips, but they are often diagnosed
creased. The main characteristic is hyper-
as such because they repeat the words to the
examiner without consonants. tonicity, normal or diminished reflexes, no

Note: Audiometer tests should be done or, in clonus, no stretch reflexes and no involun-
young children, the psychogalvanic skin resistance tary motion.
method; then, appropriately tuned hearing aids D. Ataxia-Ataxia is primary inco-ordina-
or amplifiers can be supplied to bring up the hear- lion due to disturbance of kinesthetic or
ing in that part of the sound spectrum lost.
balance sense, or both. Characterized by
G. Besides having athetosis in hearing loss, these disturbance in the sense of balance and
children have limitation of vertical eye mo-
equilibrium, dyssynengias, and the patient
tions, either upward or downward, or both,
with normal lateral eye motions. often exhibits the “rebound phenomenon”
H. Deafness, athetosis, and vertical eye motion with astereognosis and depth perception
loss, is the triad of symptoms distinguishing involvement. Atonia and hypotonia may be
the definite athetoid. present.
XI. Balance Release E. Tremor-Which may be intentional,
A. A rare type. non-intentional or constant, uncontrollable,
B. The motions
resemble exactly those which involuntary motions. of a rhythmic, alternat-
are seen individual
in walking
an in a moving ing, or pendular pattern due to alternate
train or on a loose piece of rope placed on
agonist and antagonist contractions.
the floor. Although the child is walking on a
perfecily steady floor or sidewalk, the balance F. Atonia-Lack of tone, and failure of
release mechanism comes through fully and muscles to respond to volitional stimulation.
unnecessarily. These patients seldom fall. The muscle lacks the firmness or turgor of
C. The picture is grossly the opposite of the the normal relaxed muscle. Weak stretch
ataxic gait, in which the balance motions are
reflex may be obtained as well as increased
decreased. Involuntary motions are present
in the balance release athetoid, but are absent deep reflexes, but no involuntary motion is
in the ataxic. present. This distinguishes it from non-ten-

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848 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

sion athetosis (just a matter of degree). This The evaluation of functional capacity of
is rare in pure form, but may be the initial the patient with cerebral palsy, as pre-
symptom in any of the forms of cerebral sented in this paper, is a rough estimate and
palsy. It deserves special mention because it is subject to many individual variations. In
may be the outstanding initial symptom. order to make the evaluation more scien-
The atonic form of cerebral palsy, in most tific, a careful study should be made similar
instances, does not describe a type, but the to the work of McBride on “Disability Eval-
outstanding symptoms of a type. uation.” The details of this type of evalua-
G. Mixed-The mixed class need not be tion should be worked out by specialists in
used often, as the predominant motor symp- each field in order to insure proper numeri-
toms determine the classification. cal evaluations.
The majority of members returning ques-
STATISTICAL DATA
tionnaires wanted to accept a classification
TYPES OF ATHETOSIS : The majority of the based on motor symptoms. A few members
members of the American Academy of Cere- with a good deal of experience in the field
bral Palsy approved of Tension, Non- of cerebral palsy strongly urge a simple
tension, Dystonic, and Tremor-like types of classification, e.g., (1) Pyramidal; (2) Extra-
athetosis. The others were rejected for van- pyramidal; (3) Ataxic; and (4) Mixed. One
ous reasons. Possibly, some of the other supporter of this classification feels that we
types would have been accepted if under- are likely to do more harm than good by
stood by the members, each type needs accepting one more complicated, and that
further study. (See outline of Athetosis, we must not let our classification outrun
herein.) our understanding. Many are opposed to
DISCUSSION this type on the premise that the clinician
The majority of the members of the presumes that he knows the approximate
American Academy for Cerebral Palsy ad- site of the lesion.
cept a motor classification, listing 6 sep- Most members feel that certain well nec-
arate types (7 with the mixed type), fol- ognized neurological syndromes such as the
lowed by the topographic involvement and progressive neurological diseases and neo-
etiology when this can be determined. The plastic diseases should not be included in a
chief advantage of this classification is that cerebral palsy classification, but only the
it aids the clinician in planning treatment static (non-progressive) neurological states.
of the patient with cerebral palsy. Pro- The field of cerebral palsy is now limited
ponents of this classification point out that to a more logical and manageable size.
the best a clinician can (10 15 describe the Those who prefer the descriptive or
symptoms carefully so that, eventually, symptomatic (motor) classification must
anatomical study of post-mortem material accept a stern word of warning that neuro-
can be correlated with the clinical symp- logical signs and symptoms change as the
toms. Despite its obvious faults, the motor nervous system matures and that one must
classification is practical for the clinician be extremely cautious in making a final
and for those engaged in the various phases descriptive diagnosis in infancy. (Those
of treating cerebral palsy. We cannot escape concerned are urged to read the paper by
the fact that the treatment of cerebral palsy Byers.3) For example, some infants with
is, largely, the tneatment of symptoms, not cerebral palsy may undergo a sequence of
the treatment of the etiological factor or the hypotonicity, hypertonicity, and, finally,
treatment of some specific area of the brain. athetosis, on some other extnapynamidal
The site of brain lesion is, of course, added dyskinesia as the nervous system matures.
whenever this can be determined accu- It is only when the symptoms become static,
rately, by autopsy, surgery, on other following maturation of the nervous sys-
methods. tem, that the descriptive classification is of

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 AMERICAN ACADEMY OF PEDIATRICS - SPECIAL ARTICLE 849

value. A further study of changing neuro- to school age or by comparing initial with
logical patterns during childhood and in- final neurological descriptions from first to
fancy is urgently needed. fifth year of life or later, to determine the
As it has been demonstrated that the pattern of changing neurological symptoms.
motor classification must be applied with Those who have examined large numbers
caution, until there is some degree of of children with cerebral palsy over many
maturation of the nervous system, we may years have had the disconcerting expeni-
profit by making a survey of children with ence of making a diagnosis of “atonia” only
cerebral palsy, followed from early infancy to find, in later years, that the child was

Type of Athetosi8 Approve Do P,’ot Approve No Answer

Rotary 16 7

Treiuor
1abduction-adduction
.
12
) flexion-extension

l)ystonic 27 13 5
Shudder 15 23 7
Flail(ing) 19 18 8
Tension so 9 6
Non-tension 2’ 15 8
Ilerniathetosis (topographical) 1 18 6
Neck and arm (topographical) 19 () 6
l)eaf athetoid 18 7
Balance release is s 7
Emotional release 11 24 10

Classification Based on Motor Symptoms

27 of the members preferred listing the types separately, e.g., spastic, athetoid, tremor, rigidity, ataxic, atonic,
an(l mixed.
15 of the members preferred the classification listing 3 main types of cerebral palsy: (1) Spastic (a) Atonic;
() Dyskinetic (a) Athetosis, (b) Rigidity, (c) Tremor-like; (3) Ataxic; and (4) Mixed.
3 members expressed no preference.

Classification based on Etwlegy

13 members prefer including progressive neurological diseases.
‘g members prefer deleting progressive neurological diseases.
16 members wish to include neoplastic diseases.
26 members wish to delete neoplastic diseases.

Supplemenlal Classification: These were checked as important enough to be included in the diagnosis by the follow-
jug number of members (out of 45):
35-iiitelligence quotient 36-Major sensory disturbances
3-I)evelopmental level (Gesell) 20-Physical status (comparative)
38 -Convulsive seizures 4-Posture and locomotive behavior
24 -Eye and hand behavior patterns 17-Additional behaviour ternis
32-Visual status 35-Auditory status

The returned questionnaires indicate the following choices as a basis of classification for cerebral palsy:
First choice: Motor Symptoms
Second choice : Topographic Involvement
Third choice: Etiology
Fourth choice: Anatomical Site
Fifth choice: Severity of Involvement

Sixth choice: Degree of Muscle Tone

Seventh choice: Supplemental Data

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850 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

athetoid on spastic. Atonia may be an initial In a letter dated October 20, 1954, Ada-
symptom of any one of the major types of line C. Hayden, Associate Editor of Stand-
cerebral palsy. One must look carefully for ard Nomenclature of Diseases and Opera-
involuntary motion which, if found, would tions, states,12 “. . . I would like to state that
indicate athetosis. Some feel that the atonic we expect to have a complete revision of
phase may be an initial symptom of all the the section on Neurology for the 5th ecU-
major types of cerebral palsy. Some chil- tion. At this time, the conditions which you
dren may go through rigidity with opistho- present would be coded as follows : . . . All
tonos, flaccidity and athetosis. Therefore, cerebral palsy is coded cerebral spastic in-
we must accept the fact that the motor fantile paralysis 933.4-076 with the supple-
classification in infancy is no more than a mentary terms.”
tentative appraisal. This would indicate that all types of cere-
Conditions resembling cerebral palsy in- bral palsy are caused by underdevelopment
dude such conditions as the “high cervical of the brain due to prenatal influence (see
syndrome” described by 78 These pages 49-50, Etiologic Classification, Stand-
should probably be grouped under “Spinal ard Nomenclature of Diseases and Opera-
Palsy” and the entire neurological group tions). Given the following clinical diag-
then referred to as “Cerebrospinal Palsy.” noses, the record librarian, using the pres-
The term “Cerebrospinal Palsy” is probably ent edition, would code as follows:
better than cerebral palsy for the whole Diagnosis: Cerebral palsy, spastic hemiplegia,
grouping, because it has been demonstrated etiology brain hemorrhage at birth. Coding:
that spinal lesions exist alone or in combina- 933.4-076; 94x-050 Birth injury of extrinsic
lion with brain lesions in certain types of arteries of the brain, and 969 hemiplegia.
so-called “Cerebral Palsy.” Diagnosis: Cerebral palsy athetoid quadri-
The introduction to Standard Nomencla- plegia, dystonic type, etiology unknown. Cod-
ture of Diseases and Operations,1 now in ing: 933.4-076; 9211 Athetosis; 96x Quadni-
use by medical record librarians, states: plegia, tetraplegia; 9216 Dystonic movements.
“The method of classification is based on Diagnosis: Cerebral palsy, rigidity quadniplegia,
two elements : The portion of the body con- etiology cerebral anoxia at birth. Coding:
cerned (topographic) and the cause of the dis- 933.4-076; 96x Qudaniplegia; 540 Anoxemia.
order (etiologic). These two elements are Diagnosis: Cerebral palsy, ataxic type, etiology
designated by code number separated from unknown. Coding: 933.4-076; 271 Atonia.
each other by a hyphen. The first three digits
Diagnosis: Cerebral palsy, atonic type, etiology
describe the topographic site; the last three,
unknown. Coding: 933.4-076; 272 Atonia.
following the hyphen, describe the etiologic
agent. Combined, they form a complete diag- Diagnosis: Cerebral palsy, tremor type, quadri-
nostic code number.” plegia. Coding: 933.4-076; 96x Quadniplegia;
9228 Tremor.
The above method of coding and classifica-
The proposec classification system, includ-
tion for cerebral palsy is impractical, and,
ing coding, is as follows:
in some cases, impossible, since the etiology
and the anatomical area of the brain can CEREBRAL Pu..sy “X”#{176}
only infrequently be determined accurately.
I. Physiological (motor)
The present edition of Standard Nomencla-
A. Spastic X(S)#{176}
ture of Dfiseases and Operations’ can be
B. Athetotic X9211
used for the spastic type of cerebral palsy C. Rigidity X(R)#{176}
if it is caused by a disease due to prenatal D. Ataxic .X271
influence (see page 392, line 4), however, E. Tremor .X9228
F. Atonic X272
if the spasticity is due to other causes, e.g.,
postnatal influence, or in other types of 0 Above, indicates that code number is to be
cerebral palsy, the coding is unsatisfactory. assigned.

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 AMERICAN ACADEMY OF PEDIATRICS - SPECIAL ARTICLE 851

C. Mixed X (plus any combina- lesion left by the removal of a brain tumor,
tion above) however, is still considered one of the
H. Unclassified . . .XYOO
etiological factors of cerebral palsy.
11. Topographical
Cerebral palsy comprises the motor and
A. Monoplegia . . . -948 llndicate proper
other symptom complexes caused by a non-
B. Paraplegia . . . .X . . . -94l physiological progressive brain lesion (or lesions).
C. Hemiplegia . . .X . . . -969 Icode number The nomenclature and classification ques-
1). Triplegia X . . . -978 tionnaires indicate that the members of the
E. Quadriplegia . .X . . . -96x
American Academy for Cerebral Palsy wish
Ill. Etiological (Add to diagnosis when determined) to accept a motor classification, listing each
A. Prenatal -0 type of cerebral palsy separately : Spastic,
B. Natal Anoxia -048 Athetoid, Tremor, Rigidity, Ataxic, Atonic,
C. Postnatal and Mixed.
1. Trauma -4
The following choices as a basis for
2. Infection -1
3. Toxic causes -3
classification of cerebral palsy were made
4. Vascular accidents -50 by the American Academy for Cerebral
5. Anoxia -421 Palsy:
6. Neoplastic -8 First choice: Motor Symptoms
(When coding etiology, above, indicate agent by Second choice: Topographic Involvement
proper digits).
Third choice: Etiology
Iv. Supplemental (may be coded from ‘supple- Fourth choice: Anatomical Site (of lesion)
mentary terms” in nomenclature book) Fifth choice: Severity of Involvement
A. Psychological evaluation
Sixth choice: Degree of Muscle Tone
B. Physical status
Seventh choice : Supplemental Data
C. Convulsive seizures
D. Posture and locomotive behaviour pattern The first 3 choices above should be used
E. Eye-hand behaviour pattern by the medical record librarian and by
F. Visual status doctors discharging patients with cerebral
C. Auditory status palsy from hospitals or institutions so as to
H. Speech disturbances
establish a common understanding and uni-
V. Neuroanatomical (select code number from formity to hospital records. It is under-
“Brain,” pp. 38-39-40’) stood that the neuroanatomical classifica-

VI. Functional Capacity (degree of severity)

tion (Fourth choice) is to be used when it
can be proven, but not by presumption.
Class I The majority of the members approve of
Class II
tension, non-tension, dystonic, and tremor-
Class III
like types of athetosis. The other types were
Class IV
rejected for various reasons. Probably, some
VII. Therapeutic
of the other types would have been ac-
Class A
cepted if understood by the members. Each
Class B
Class C
type is described and defined herein. There
Class D is a general lack of agreement on the van-
(Note: VI and VII, above, need not be coded by
ous terms used in cerebral palsy. Defini-
librarian, but added to the final diagnosis.) tions of these terms are now being made
by a committee for a meeting in 1955.
CONCLUSIONS There is a good deal of evidence that
The majority of the members of the neurological signs and symptoms change in
American Academy for Cerebral Palsy voted the child with cerebral palsy as the nervous
to exclude progressive neurological diseases system matures and that one must be cau-
and neoplastic diseases of the brain from tious in making a final descriptive or symp-
the classification of cerebral palsy. The tomatic diagnosis in infancy. The pattern of

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852 MINEAR - CLASSIFICATION OF CEREBRAL PALSY

changing neurological symptoms from in- sophical Method. Oxford, Clarendon,

fancy through childhood should be studied. 1933, pp. 26-53.
5. Fay, T. : Cerebral palsy; medical con-
The high cervical syndrome described by
siderations and classification. Am. J.
Fay is being confused with cerebral palsy. Psychiat., 107:180, 1950.
This syndrome needs further study. It 6. Cruickshank, W. M., and Raus, G. M.,
should be determined whether the term editors: Cerebral Palsy; Its Individual
cerebrospinal palsy would not be more ap- and Community Problems. Syracuse,
Syracuse Univ. Press, 1955.
propniate for the entire neurological group.
7. Fay, T. : Problems of rehabilitation in pa-
The American Medical Association’s
tients with cerebral palsy. Delaware
Standard Nomenclature of Diseases and State M. J., 18:57, 1946.
Operations (Fourth Edition), commonly 8. Hillman, J. W., Sprofkin, B. E., and Par-
used by medical record librarians, is not rish, T. F. : Birth injury of the cervical
spine producing a “cerebral palsy”
suitable for the classification of cerebral
syndrome. Am. Surgeon, 20:900, 1954.
palsy. In this edition, all cerebral palsy is
9. Fay, T. : Personal communication.
coded “Cerebral spastic infantile paralysis” 10. Gesell, A., and Amatruda, C. : Develop-
with supplementary terms added to denote mental Diagnosis, 2nd Ed. New York,
various types. Hoeber, 1947.
A complete classification for cerebral 11. Cuibor, G. P. : Personal communication.
12. Keats, S. : Cerebral palsy; recent advances
palsy is presented, using the majority opin-
in diagnosis and classification. J. M. Soc.
ion from questionnaires sent to the mem- New Jersey, 45:491, 1948.
hers of the American Academy for Cerebral 13. Minear, W. L. : Cerebral palsy; spasticity.
Palsy during 1953 as a basis. Rocky Mountain M. J., 48:757, 1951.
14. Ibid.: Cerebral palsy. Southwestern Med.,
31:367, 1950.
REFERENCES 15. Minear, W. L., Binkley, E., and Snow,
W. B. : Report, Nomenclature and Classi-
1. American Medical Association: Standard
fication Committee, presented before
Nomenclature of Diseases and Opera-
American Academy for Cerebral Palsy,
tions, 4th Ed., Plunkett, R. J., editor.
New York, Blakiston, 1952. November, 1954.
16. McBride, E. : Personal communication.
2. Balf, C. L., and Ingram, T. T. S. : Problems
17. Perlstein, M. A. : Infantile cerebral palsy;
in the classification of cerebral palsy in
classffication and clinical correlations.
childhood. Brit. M. J., 2:163, 1955. J.A.M.A., 149:30, 1952.
3. Byers, R. K. : Evolution of hemiplegias in 18. Perlstein, M. A. : Personal communication.
infancy. Am. J. Dis. Child., 61:915, 19. Phelps, W. : Personal communication.
1941. 20. Pohi, J. F. : Cerebral Palsy. St. Paul. Bruce
4. Collingwood, R. C. : An Essay on Philo- Pub. Co.. 1950.

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 SPECIAL ARTICLE: A CLASSIFICATION OF CEREBRAL PALSY
W. L. Minear
Pediatrics 1956;18;841

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 SPECIAL ARTICLE: A CLASSIFICATION OF CEREBRAL PALSY
W. L. Minear
Pediatrics 1956;18;841

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