4. Clinical features and classification of cerebral palsy

The classification of CP is based on the type and distribution of motor abnormalities. Suggestive signs and symptoms may be present in infancy, and severe cerebral palsy can be diagnosed as early as 1 month of age. However, the specific CP syndromes are best recognized in time as the child's brain matures, e.g., spastic CP is usually diagnosed after the age of 6 months, dyskinetic CP usually after 18–20 months old, and the ataxic type even later. Following-up the children with high risk will allow early recognition and intervention.

Early diagnosis, in some cases, will enable early intervention for the child by a multidisciplinary team and in addition early psychological and possible financial support to the family.

Early signs of CP include as follows:

Neurobehavioral findings: a neonate who presents with poor feeding with or without recurrent vomiting, irritability, poor sleeping pattern, and poor visual attention should raise suspicion of CP. In addition, prolonged retention or exaggeration of these primitive reflexes is often a premature sign of motor disability. In infants with hyperactive tonic labyrinthine reflex, opisthotonus may occur, or they may roll over at an earlier age than usually expected. Similarly, children with CP may present inadequate posture in vertical suspension in that they present persistent extension of lower extremities on attempting a sitting position.

Motor tone and posture: Tone can be normal in some subjects, but it may be increased or decreased in the extremities of others.

Delay in sitting without support beyond 9 months, poor head control, persistent or asymmetric hand fisting beyond 4 months, and abnormal oromotor patterns (tongue thrusting or grimacing) are often the early motor signs. Sometimes increased neck extensor and axial tone may make head control appears better than it is.

The abovementioned features may also coincide with intellectual impairment, hemianopia, and other visual problems. Also, behavioral problems are frequently found among children with hemiplegic CP including anxiety and specific phobias.

After age 18–24 months, signs and symptoms generally align to a specific subtype of CP:

Spastic CP includes spastic diplegia, spastic hemiplegia, and spastic quadriplegia, with accompanying features pointing to an upper motor neuron syndrome like spastic hypertonia, hyperreflexia, extensor plantar responses, and Dyskinetic CP is characterized by involuntary, stereotyped, uncontrolled, recurring movements of athetosis, chorea, and dystonia.

CP associated with ataxic movements (loss of orderly muscular coordination, unstable gait) and speech is referred to as ataxic CP and is usually associated with a widespread disorder of motor function. Ataxic CP is rare, and children who present with these findings must be evaluated for other potential causes of ataxia.

Mixed CP is a spastic type with ataxic and/or dyskinetic features of variable predominance.

Hypotonic CP is not included in the contemporary classifications. Majority of patients with "hypotonic CP" in early infancy later develop spastic, dyskinetic, or ataxic CP. Table 1 shows the proportion of the different types of CP.


• Gray matter damage: central gray matter damage of acute perinatal hypoxia-

• Enlarged ventricles, bilateral or unilateral, abnormalities of the atria and ventricular or occipital horns, and posterior fossa, atrophy, and cerebrospinal

In a European cerebral palsy study [14], MRI was performed in 351 of the 431 children with clinically assessed CP. The MRI scans showed that white matter damage of immaturity, including periventricular leukomalacia, was the most common finding (42.5%, majority born before 34 weeks), followed by basal ganglia lesions (12.8%), cortical/subcortical lesions (9.4%), malformations (9.1%), focal infarcts (7.4%), and

MRI scan does provide useful information on the timing and extent of the lesion.

miscellaneous lesions (7.1%). Normal MRI findings were present in 11.7%.

Salient MRI changes in cerebral palsy. Panel A shows a T2-weighted image with periventricular hyperintensities and undulating ventricular margins (solid arrow). This is typically seen in prematurity associated insult and commonly manifests as spastic diplegia. Panel B shows multicystic encephalomalacia (dotted line with arrow). This pattern of watershed lesions is seen commonly in term infants with ischemia/ asphyxia and manifests clinically with spastic quadriplegia. Panel C illustrates T2 hyperintensities in posterior putamen (open arrow) and thalami bilaterally (dotted line with closed arrow). This is typically seen in infants with term hypoxic ischemic encephalopathy (HIE) and manifests as dyskinetic cerebral palsy. Panel D highlights T2 hyperintensities in occipital lobe (solid arrow); characteristic of neonatal hypoglycemic insult. Panel E shows T2 hyperintensity involving bilateral globuspallidi (open arrow), a feature of kernicterus

Predisposing risk factors include maternal and child genetic factors in thrombophilia leading to stroke, nutritional factors, and infections during

ischemia in term infants is associated with death and CP.

fluid abnormalities [13].

DOI: http://dx.doi.org/10.5772/intechopen.82804

Epilepsy and Cerebral Palsy

Figure 1.

sequelae.

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Table 1.

Proportion of the different types of cerebral palsy.
