**3. Traditional classifications of CP based on single characteristics**

The traditional classifications of CP are basically the Minear [7] classifications in seven axes namely:

**1.** Physiological

These classifications (groups) differ in the characteristic(s) used and their individual uses or purposes. A classification may be used for describing the nature of the disability, for predicting current and future management needs, comparing cases in different areas and assessing change following an intervention [1]. Generally, it is desirable that any classification used should be

Besides early identification and intervention, the current trend in neurodevelopmental pediatrics is a focus on functional effects of different states of health [3, 4]. This is the outcome of the recent WHO International Classification of Functioning, Disability and Health (ICF) which in the field of CP led to the development of newer measures of functional abilities (functional scales) [3, 4]. There are functional scales for a number of functions impaired in CP. It is widely accepted that the functional classification remains the best classification for a

Some factors that influence the clinical classification of CP are the age of a child, reliability of the medical history, and extent of diagnostic investigations [1]. This means that the same child may be classified differently at different times (due to changes in peripheral manifestations with age), by different people (due to variable historical data from maternal recall or case notes), and in different regions (due to differences in availability and affordability of neuroimaging and metabolic studies). Therefore, Bax et al. [1] in 2005 proposed that all classification

Children with CP differ clinically in the following characteristics: type/nature of motor disorder, distribution of motor impairment, etiology, presence/number of accompanying impairments, structural brain abnormalities on neuroimaging, degree of severity of impairments, and individual therapeutic needs. These clinical variables form the basis of the traditional classifications of CP. In 1956, Minear [7] and the Nomenclature and Classification Committee of the American Academy for cerebral palsy classification put forward an early classification system that presented seven classification axes based on the aforementioned

Subsequent classification systems originated from the Minear classifications and are either a combination or an expansion of the categories. Such classification systems based on multiple variables include the Swedish classification system [8], Edinburgh classification [9] and clas-

The current emphasis on the functional consequences of different health states increased interest and research on the functional classification of CP [1, 3, 4]. The result is an evolution of newer measures (functional scales) that objectively and reliably measure and quantify functional abilities. A number of these functional scales have been validated by multiple studies [11–16]. They include Gross Motor Function Classification System (GMFCS) [11] (functional mobility/ambulatory function), Manual Ability Classification System (MACS) [14] (hand and

reliable, valid, quantitative, and objective and most importantly assist management [1].

patient with CP because it guides management [1, 5, 6].

22 Cerebral Palsy - Clinical and Therapeutic Aspects

**2. Overview of clinical classification of CP**

features.

results should indicate these factors at the time of classification.

sification by the Surveillance for Cerebral Palsy in Europe (SCPE) [10].


#### **3.1. Physiologic classification**

This is based on the type/nature of motor or movement disorder (quality and changes in tone) and classifies CP into two types: spastic (pyramidal) and non-spastic (extrapyramidal). Generally speaking, neuromotor findings in spastic CP are consistent and persistent while variability is the rule in extrapyramidal CP [6, 18, 19].

The clinical features of spastic CP are as follows [6, 18, 19]:

• Tone is invariably increased (hypertonia), that is, persistently increased with little or no variation in the awake (movement, tension and emotion) or sleep states. This is further confirmed by asking caregivers whether their child feels stiff when touched or held most times of the day even during sleep. The answer is usually a "yes."

• The quality of the increased tone is described as "clasp-knife" spasticity and is elicited clinically by a rapid passive movement at a joint (as rapidly as the time taken to say "one thousand and one"). This produces the classic "clasp-knife" resistance followed by a sudden "give." Spasticity refers to hypertonia due to a velocity-dependent increase in tonic spinal stretch reflex.

the distal parts of the body (extremities) (athetosis) and usually with reduced tone. This is the commonest type of extrapyramidal CP. Dystonic CP is characterized by extrapyramidal hypertonia and decreased movement (hypokinesia). Dystonia occurs when there is simultaneous contraction of both agonist and antagonist muscles. Ataxic CP occurs when there are signs of incoordination and hypotonia caused by damage to the cerebellum. This

Clinical Classification of Cerebral Palsy http://dx.doi.org/10.5772/intechopen.79246 25

One merit of the physiological classification is that it can suggest the areas of brain damage and possible etiological factors. For instance, spasticity would suggest damage to the cortical neurons (pyramidal cells) due to hypoxic ischemic encephalopathy (HIE) from severe perinatal asphyxia and postnatal central nervous system (CNS) infections like meningitis [19]. In addition, dyskinetic CP points to damage to the basal nuclei by bilirubin encephalopathy and severe perinatal asphyxia at term [19]. Therefore, the physiological classification is still

However, the physiological classification is not reliable [6, 18, 20]. The terms spastic (pyramidal) and extrapyramidal CP are strictly incorrect [6, 18, 20]. It is more accurate to refer to these as "predominantly spastic" and "predominantly non-spastic." Due to the complex interactions of the upper motor neuron system (the pyramidal, extrapyramidal, and cerebellar pathways) with the anterior horn cells to control posture and movement, lesions causing CP in real life usually involve both pyramidal and extrapyramidal pathways [21]. Strictly speaking, pyramidal lesions induce spasticity as a result of concomitant damage to extrapyramidal pathways [21]. This explains the clinical combination of motor/movement abnormalities, for example, spasticity and dystonia, and spasticity and choreoathetosis. This is the so-called mixed CP subtype. From the explanation above, this CP subtype should actually be very common but from published studies [22, 23], spastic CP remains the commonest type thereby exposing the subjectivity and imprecision in assessment of patients based on this classification. Additionally, the physiological classification does not aid therapy or inform management of patients with CP, and this inability to indicate functional abilities remains a

This classification relies on the localization/limb distribution of neuromotor impairment in spastic CP [19]. It subdivides spastic CP into: quadriplegia (symmetric/equal and severe spasticity of all four limbs), diplegia (involvement of the four limbs but greater spasticity and weakness in the lower limbs) and hemiplegia (involvement of the upper and lower limbs on one side of the body) [19]. Other types of spastic CP such as tripegia (three-limb spasticity) and monoplegia (one-limb spasticity) are rare, and double hemiplegia (four extremity

An advantage of this classification is that these topographical subtypes can be linked to some etiological factors. For instance, diplegia suggests periventricular leukomalacia due to prematurity/low birth weight; hemiplegia suggests perinatal stroke, periventricular hemorrhagic infarction or neonatal cortical infarction while quadriplegia suggests severe perinatal

involvement with greater spasticity of the upper limbs) is no longer in use [6, 20].

is a rare form of CP [6, 18, 19].

clinically useful.

major drawback [6, 18, 20].

**3.2. Topographic classification**


In contrast, the clinical features of extrapyramidal (non-spastic) CP are [6, 18, 19]:


the distal parts of the body (extremities) (athetosis) and usually with reduced tone. This is the commonest type of extrapyramidal CP. Dystonic CP is characterized by extrapyramidal hypertonia and decreased movement (hypokinesia). Dystonia occurs when there is simultaneous contraction of both agonist and antagonist muscles. Ataxic CP occurs when there are signs of incoordination and hypotonia caused by damage to the cerebellum. This is a rare form of CP [6, 18, 19].

One merit of the physiological classification is that it can suggest the areas of brain damage and possible etiological factors. For instance, spasticity would suggest damage to the cortical neurons (pyramidal cells) due to hypoxic ischemic encephalopathy (HIE) from severe perinatal asphyxia and postnatal central nervous system (CNS) infections like meningitis [19]. In addition, dyskinetic CP points to damage to the basal nuclei by bilirubin encephalopathy and severe perinatal asphyxia at term [19]. Therefore, the physiological classification is still clinically useful.

However, the physiological classification is not reliable [6, 18, 20]. The terms spastic (pyramidal) and extrapyramidal CP are strictly incorrect [6, 18, 20]. It is more accurate to refer to these as "predominantly spastic" and "predominantly non-spastic." Due to the complex interactions of the upper motor neuron system (the pyramidal, extrapyramidal, and cerebellar pathways) with the anterior horn cells to control posture and movement, lesions causing CP in real life usually involve both pyramidal and extrapyramidal pathways [21]. Strictly speaking, pyramidal lesions induce spasticity as a result of concomitant damage to extrapyramidal pathways [21]. This explains the clinical combination of motor/movement abnormalities, for example, spasticity and dystonia, and spasticity and choreoathetosis. This is the so-called mixed CP subtype. From the explanation above, this CP subtype should actually be very common but from published studies [22, 23], spastic CP remains the commonest type thereby exposing the subjectivity and imprecision in assessment of patients based on this classification. Additionally, the physiological classification does not aid therapy or inform management of patients with CP, and this inability to indicate functional abilities remains a major drawback [6, 18, 20].

#### **3.2. Topographic classification**

• The quality of the increased tone is described as "clasp-knife" spasticity and is elicited clinically by a rapid passive movement at a joint (as rapidly as the time taken to say "one thousand and one"). This produces the classic "clasp-knife" resistance followed by a sudden "give." Spasticity refers to hypertonia due to a velocity-dependent increase in tonic

• A positive Babinski sign (extensor planter response), that is, lightly stroking the lateral aspect of the sole and across the foot pads/ball of the foot, results in extension/dorsiflexion

• Sustained ankle clonus, that is, when the ankle is briskly dorsiflexed on a flexed knee, a

• Localization/limb distribution of neuromotor impairment varies from one child to another

• Tone is variably increased (varies from hypertonia to hypotonia) depending on the state, that is, tone is increased by activity, agitation, tension, and emotions like crying, but tone is decreased in sleep and when relaxed. Caregiver usually tells the clinician that their child

• The quality of the increased tone is "lead pipe" rigidity or "candle wax" type and is elicited clinically by a slow passive flexion and extension of a limb. The increased resistance to this passive movement is felt all through the movement. Besides, extrapyramidal hypertonus

• Positional contractures (the variable tone is protective against contractures and so contractures like hip/knee flexion contracture only occur after prolonged periods on a wheelchair).

• There is a four-limb functional impairment that precludes further topographic classification. However, extrapyramidal or dyskinetic CP is further subdivided based on the different manifestations of abnormal/involuntary movements (dyskinesia) and tone. The subtypes are choreathetoid CP—characterized by excessive and rapid movements involving the proximal body parts (trunk) (chorea) combined with slow writhing movements of

• Deep tendon reflexes are markedly increased (more commonly grade 3+ or 4+)

of the hallux (up-going big toe) and fanning out/spreading of the other toes.

In contrast, the clinical features of extrapyramidal (non-spastic) CP are [6, 18, 19]:

can be diminished by repetitive movement and this is called "shaking it out."

• Deep tendon reflexes are usually normal or mildly increased (grade 1+ to 3+).

• Movement is disordered. Thus, extrapyramidal CP is also called dyskinetic CP.

spinal stretch reflex.

24 Cerebral Palsy - Clinical and Therapeutic Aspects

• Decreased movement

• A negative Babinski sign. • Unsustained ankle clonus.

rhythmic contraction is observed.

limbs feel normal when asleep or quiet.

• Non-positional contractures (due to persistent hypertonia)

and so spastic CP can be further classified topographically.

This classification relies on the localization/limb distribution of neuromotor impairment in spastic CP [19]. It subdivides spastic CP into: quadriplegia (symmetric/equal and severe spasticity of all four limbs), diplegia (involvement of the four limbs but greater spasticity and weakness in the lower limbs) and hemiplegia (involvement of the upper and lower limbs on one side of the body) [19]. Other types of spastic CP such as tripegia (three-limb spasticity) and monoplegia (one-limb spasticity) are rare, and double hemiplegia (four extremity involvement with greater spasticity of the upper limbs) is no longer in use [6, 20].

An advantage of this classification is that these topographical subtypes can be linked to some etiological factors. For instance, diplegia suggests periventricular leukomalacia due to prematurity/low birth weight; hemiplegia suggests perinatal stroke, periventricular hemorrhagic infarction or neonatal cortical infarction while quadriplegia suggests severe perinatal asphyxia at term, postnatal infection (bacterial meningitis) and metabolic/genetic disorders [19]. However, the descriptive terms in the topographic classification cannot be used reliably [6, 20]. One notable source of confusion is distinguishing spastic diplegia from quadriplegia. This distinction is highly subjective since it is unclear how much upper limb spasticity is needed to separate a diplegia from a quadriplegia [6, 20]. Recall that there is involvement of the four limbs in both subtypes. The arm and leg naturally perform different functions, and assessing the relative severity of involvement is difficult [1]. Moreover, the imprecise use of these terms in clinical practice has been reported by Gorter et al. [24] Many experts agree that the use of these terms in classification should be stopped [1]. Furthermore, the topographic classification does not consider functional abilities and so does not aid therapy or inform management of these children [6, 20]. Therefore, the topographic and physiological classifications share similar merits and demerits.

**3.4. Etiologic classification**

postnatal [6, 19, 20].

kernicterus.

The categorization based on the actual cause (etiology) and timing of insult was aimed at prevention, and the association of erythroblastosis fetalis with choreoathetoid CP was the paradigm for this classification [6, 20]. The etiology of CP is multifactorial, and the causal pathways are (mechanisms) multiple and complex. The Collaborative Perinatal Project [25] identified the associated risk factors for CP. Due to the fact that much of the data in these epidemiological studies [25, 26] are still correlational, "risk factors" are more appropriate than etiology. These risk factors or associated etiological factors in CP include genetic abnormalities, cerebral dysgenesis, multiple gestation, intrauterine/congenital infection (TORCHS), maternal infection (UTI), prematurity, low birth weight, perinatal asphyxia (HIE), bilirubin encephalopathy, postnatal CNS infections, etc. [19, 25, 26]. These associated etiological factors can be classified according to the timing of insult as prenatal (commonest), perinatal and

Clinical Classification of Cerebral Palsy http://dx.doi.org/10.5772/intechopen.79246 27

Identifying both the disturbances or events and causal pathways or processes that led to the damage to the developing motor system remains a challenge [6, 20]. This is compounded by the fact that most of these factors are prenatal in timing. Therefore, the etiological classifica-

This classification correlates specific radiologic findings (brain structural alterations) with types of CP [6, 20]. This implies categorizing CP patients based on neuroradiologic findings. Thus, the neuropathologic classification relies on neuroimaging studies such as magnetic

Neuroimaging contributes significantly to the understanding of the etiology and pathology of CP and the timing of insults [1, 6, 20]. In a systematic review of neuroimaging for cerebral palsy, Korzeniewski et al. [27] classified abnormal radiological findings and diagnoses into five categories namely: malformations, gray matter damage, white matter damage, ventricu-

Though the correlations between the neuropathologic substrates and clinical types have been weak and inconsistent, recent advances such as diffusion tensor imaging, magnetic resonance spectroscopy, functional magnetic resonance imaging and fast spin echo imaging have improved greatly the possibility of a comprehensive radiologic classification [6, 20, 27]. A recent study by Hou et al. [28] continues to correlate neuropathologic findings with different clinical types of CP. For example, dyskinesia correlated with lesions detected by MRI in the thalamus and putamen due to HIE and in the globus pallidus and hypothalamus due to

There are also difficulties in estimating the timing of insults in CP using neuroimaging findings. It was initially assumed that the presence of neuronal migrational disorders meant that the insult occurred in the first half of pregnancy while the presence of a glial response indicated insults around the second half of pregnancy [27]. However, there is evidence that cell

tion was severely limited and failed in addressing prevention [6, 20].

resonance imaging (MRI) and computed tomography scan (CT scan).

lomegaly, atrophy or CSF space abnormalities and miscellaneous findings.

**3.5. Neuroanatomic (neuropathologic) classification**

#### **3.3. Supplemental classification**

This is an additional grouping that comprises the accompanying impairments in CP and their association with the physiological and topographic classifications [6, 20]. The accompanying physical, mental or physiological impairments in CP include epilepsy, cognitive (intellectual), speech, visual and hearing impairments, behavioral problems and secondary musculoskeletal abnormalities (hip dislocation/subluxation, contractures) [1, 2]. The purpose of linking these supplemental disorders to the physiological and topographic classifications was to identify syndromes with a common etiology that would lead to prevention [6, 20]. Unfortunately, the supplemental disorders correlated poorly with the two earlier classifications. This means that it was only in a few examples like bilirubin encephalopathy that such a link between supplemental disorders, physiology and etiological factor could be established. For instance, the combination of accompanying impairments—vertical gaze palsy, sensorineural deafness and enamel dysplasia—is associated with choreoathetoid CP (physiology) from damage to the basal nuclei by bilirubin encephalopathy (etiological factor) [6, 20].

Though these associations were limited and the aim of the supplemental classification defeated, supplemental disorders (accompanying impairments) remain pertinent to the current management of CP because their presence strengthens the need for multidisciplinary management. This means that the accompanying impairments need to be taken into consideration in planning service delivery. Moreover, the accompanying impairments may cause more functional limitation than the primary motor dysfunction (the core feature of CP) and thus must be addressed to achieve a positive functional outcome. Furthermore, the most recent definition of CP [2] highlights the importance of these accompanying impairments by incorporating them as part of the definition of CP since CP rarely occurs without them. It is generally recommended that the presence or absence of these impairments and the extent to which they interfere with function be recorded in addition to the classifications used [1]. Currently, it is recommended that at least the presence/absence of epilepsy be recorded and intellectual function (IQ), vision and hearing be assessed [1].

#### **3.4. Etiologic classification**

asphyxia at term, postnatal infection (bacterial meningitis) and metabolic/genetic disorders [19]. However, the descriptive terms in the topographic classification cannot be used reliably [6, 20]. One notable source of confusion is distinguishing spastic diplegia from quadriplegia. This distinction is highly subjective since it is unclear how much upper limb spasticity is needed to separate a diplegia from a quadriplegia [6, 20]. Recall that there is involvement of the four limbs in both subtypes. The arm and leg naturally perform different functions, and assessing the relative severity of involvement is difficult [1]. Moreover, the imprecise use of these terms in clinical practice has been reported by Gorter et al. [24] Many experts agree that the use of these terms in classification should be stopped [1]. Furthermore, the topographic classification does not consider functional abilities and so does not aid therapy or inform management of these children [6, 20]. Therefore, the topographic and physiological classifica-

This is an additional grouping that comprises the accompanying impairments in CP and their association with the physiological and topographic classifications [6, 20]. The accompanying physical, mental or physiological impairments in CP include epilepsy, cognitive (intellectual), speech, visual and hearing impairments, behavioral problems and secondary musculoskeletal abnormalities (hip dislocation/subluxation, contractures) [1, 2]. The purpose of linking these supplemental disorders to the physiological and topographic classifications was to identify syndromes with a common etiology that would lead to prevention [6, 20]. Unfortunately, the supplemental disorders correlated poorly with the two earlier classifications. This means that it was only in a few examples like bilirubin encephalopathy that such a link between supplemental disorders, physiology and etiological factor could be established. For instance, the combination of accompanying impairments—vertical gaze palsy, sensorineural deafness and enamel dysplasia—is associated with choreoathetoid CP (physiology) from damage to the basal nuclei by bilirubin encephalopathy (etiological

Though these associations were limited and the aim of the supplemental classification defeated, supplemental disorders (accompanying impairments) remain pertinent to the current management of CP because their presence strengthens the need for multidisciplinary management. This means that the accompanying impairments need to be taken into consideration in planning service delivery. Moreover, the accompanying impairments may cause more functional limitation than the primary motor dysfunction (the core feature of CP) and thus must be addressed to achieve a positive functional outcome. Furthermore, the most recent definition of CP [2] highlights the importance of these accompanying impairments by incorporating them as part of the definition of CP since CP rarely occurs without them. It is generally recommended that the presence or absence of these impairments and the extent to which they interfere with function be recorded in addition to the classifications used [1]. Currently, it is recommended that at least the presence/absence of epilepsy be recorded and intellectual function (IQ), vision and hearing be

tions share similar merits and demerits.

**3.3. Supplemental classification**

26 Cerebral Palsy - Clinical and Therapeutic Aspects

factor) [6, 20].

assessed [1].

The categorization based on the actual cause (etiology) and timing of insult was aimed at prevention, and the association of erythroblastosis fetalis with choreoathetoid CP was the paradigm for this classification [6, 20]. The etiology of CP is multifactorial, and the causal pathways are (mechanisms) multiple and complex. The Collaborative Perinatal Project [25] identified the associated risk factors for CP. Due to the fact that much of the data in these epidemiological studies [25, 26] are still correlational, "risk factors" are more appropriate than etiology. These risk factors or associated etiological factors in CP include genetic abnormalities, cerebral dysgenesis, multiple gestation, intrauterine/congenital infection (TORCHS), maternal infection (UTI), prematurity, low birth weight, perinatal asphyxia (HIE), bilirubin encephalopathy, postnatal CNS infections, etc. [19, 25, 26]. These associated etiological factors can be classified according to the timing of insult as prenatal (commonest), perinatal and postnatal [6, 19, 20].

Identifying both the disturbances or events and causal pathways or processes that led to the damage to the developing motor system remains a challenge [6, 20]. This is compounded by the fact that most of these factors are prenatal in timing. Therefore, the etiological classification was severely limited and failed in addressing prevention [6, 20].

#### **3.5. Neuroanatomic (neuropathologic) classification**

This classification correlates specific radiologic findings (brain structural alterations) with types of CP [6, 20]. This implies categorizing CP patients based on neuroradiologic findings. Thus, the neuropathologic classification relies on neuroimaging studies such as magnetic resonance imaging (MRI) and computed tomography scan (CT scan).

Neuroimaging contributes significantly to the understanding of the etiology and pathology of CP and the timing of insults [1, 6, 20]. In a systematic review of neuroimaging for cerebral palsy, Korzeniewski et al. [27] classified abnormal radiological findings and diagnoses into five categories namely: malformations, gray matter damage, white matter damage, ventriculomegaly, atrophy or CSF space abnormalities and miscellaneous findings.

Though the correlations between the neuropathologic substrates and clinical types have been weak and inconsistent, recent advances such as diffusion tensor imaging, magnetic resonance spectroscopy, functional magnetic resonance imaging and fast spin echo imaging have improved greatly the possibility of a comprehensive radiologic classification [6, 20, 27]. A recent study by Hou et al. [28] continues to correlate neuropathologic findings with different clinical types of CP. For example, dyskinesia correlated with lesions detected by MRI in the thalamus and putamen due to HIE and in the globus pallidus and hypothalamus due to kernicterus.

There are also difficulties in estimating the timing of insults in CP using neuroimaging findings. It was initially assumed that the presence of neuronal migrational disorders meant that the insult occurred in the first half of pregnancy while the presence of a glial response indicated insults around the second half of pregnancy [27]. However, there is evidence that cell migrational disorders can occur in the last 2–3 months of pregnancy [27]. Nevertheless, malformations are more likely to occur earlier in gestation, and thus, neuroimaging confirmation of their presence can help establish that the cause of CP is unrelated to perinatal events [27].

important descriptive information. Besides, it does not indicate supplemental disorders that

Clinical Classification of Cerebral Palsy http://dx.doi.org/10.5772/intechopen.79246 29

Iloeje and Ogoke [29] in 2017 reported that the type of CP (physiology and topography), etiological factors and the number of accompanying impairments (supplemental disorders) were positively associated with the severity of gross motor dysfunction and walking ability of children with CP. In that study [29], children with spastic quadriplegic type, bacterial meningitis as etiological factor or many (five or six) accompanying impairments all had severe gross motor dysfunction and were non-ambulatory. Therefore, the other classifications may

These are the Swedish classification [8], Edinburgh classification [9] and Surveillance for

CP subtypes based on the Swedish classification (1989) [8] are spastic (hemiplegic, tetraplegic, and diplegic), dyskinetic (dystonic and athetotic), ataxic and unclassified/mixed. It is immediately obvious that this classification combines the Minear's Physiologic and Topographic schema. Thus, it shares the same merits and demerits as the physiological and topographic

According to the Edinburgh classification [9], there are six subtypes of CP namely hemiplegia, bilateral hemiplegia, diplegia, ataxic, dyskinetic and other forms of CP including mixed forms. This classification is a combination of classifications based on topography and physiology and so has the same advantages and shortcomings as the topographic and physiologic

The SCPE [10] classifies CP into the following four subtype groups: spastic (bilateral and unilateral), dyskinetic (dystonic and choreoathetotic), ataxic, and non-classifiable. This grouping also combines the physiological and topographic classifications. The classification tree of the

Due to the lack of reliability of the terms used in Minear's topographic classification, SCPE [10] introduced two new terms to replace quadriplegia, diplegia, and hemiplegia. These terms are bilateral and unilateral used to describe involvement of both sides and one side of the body, respectively. By this classification, spastic quadriplegia and spastic diplegia are classified as bilateral spastic CP (BS-CP) while spastic hemiplegia is termed unilateral spastic CP. This

**4.3. The Surveillance for Cerebral Palsy in Europe (SCPE) classification**

are necessary for assessing the service delivery needs of patients with CP.

**4. Traditional classifications of CP based on multiple variables**

suggest functional abilities in children with CP.

Cerebral Palsy in Europe (SCPE) classification [10].

**4.1. The Swedish classification**

classifications as earlier discussed.

**4.2. The Edinburgh classification**

SCPE for subtypes of CP is shown in **Figure 1**.

classifications.

Categorizing patients with CP based on neuroradiologic findings implies that neuroimaging studies be carried out on all patients. Therefore, it will be difficult to apply such classification in resource-poor countries where neuroimaging facilities are not readily available or affordable and the professional expertise needed may be lacking. Despite this, the American Academy of Neurology (AAN) recommends neuroimaging studies on all children with CP whenever possible [27]. The bottom line is that neuroimaging can be used to identify the neuropathologic substrates of the various etiologic and risk factors of CP, possibly provide information about timing of insults and detect cerebral dysgenesis or malformations but, at present, a comprehensive neuropathologic classification is still in the pipeline.

#### **3.6. Therapeutic classification**

This scheme categorizes CP cases based on treatment needs into four groups namely: nontreatment, modest treatment, need for a CP treatment team, and pervasive support groups [6, 20]. Parents/caregivers want their children to receive treatments that will improve their condition, so any classification that is implicative of treatment is important to the patients and their caregivers and relevant to clinical practice. There is a consensus in the literature that the therapeutic and functional classifications are the most important to the patient [1, 6, 20].

However, the therapeutic classification simply identifies how much treatment or the extent of interventions a given child requires without specifying what is actually needed to improve function. This explains the little emphasis on the therapeutic classification.

#### **3.7. Functional classification**

Functionally, CP is classified into levels of severity based on functional (motor) abilities and/ or limitation of activity [1, 6, 20]. Currently, the emphasis on the functional classification is due to its important role in the management of CP. So there is a rekindled interest in this scheme.

The functional classification remains the best classification of CP because it is a useful guide to providing care for patients appropriate for their functional level and helps clinicians set and discuss with parents/caregivers realistic rehabilitation goals [1, 4, 5, 11, 12]. The functional classification satisfies the needs of patients and parents/caregivers by informing the current and future service needs of children with CP [5]. It provides information that will permit comparison of CP cases in different locations. It provides information that will allow evaluation of change at different points in time in the same patient such as after an intervention [1].

However, it falls short of giving full descriptive information about a child with CP that clearly delineates the nature of the problem. It does not indicate the nature of the motor abnormality, the topography, the etiology, or neuropathologic substrates which in their own respects are important descriptive information. Besides, it does not indicate supplemental disorders that are necessary for assessing the service delivery needs of patients with CP.

Iloeje and Ogoke [29] in 2017 reported that the type of CP (physiology and topography), etiological factors and the number of accompanying impairments (supplemental disorders) were positively associated with the severity of gross motor dysfunction and walking ability of children with CP. In that study [29], children with spastic quadriplegic type, bacterial meningitis as etiological factor or many (five or six) accompanying impairments all had severe gross motor dysfunction and were non-ambulatory. Therefore, the other classifications may suggest functional abilities in children with CP.
