J Dev Phys Disabil (2009) 21:153167 DOI 10.

1007/s10882-009-9130-3 R E V I E W A RT I C L E

Effects of Cerebral Palsy on Neuropsychological Function

Kathryn Straub & John E. Obrzut

Published online: 23 January 2009 # Springer Science + Business Media, LLC 2009

Abstract Cerebral Palsy (CP) is a muscle and movement disorder that affects children and is the result of early brain injury. The causes and nature of the brain damage may vary considerably, which renders children with cerebral palsy a heterogeneous group. Only recently has research begun to utilize technology to determine the nature of the brain injury and the relation to clinical observations. This paper reviews neuropsychological findings on children with a diagnosis of CP with regard to the spastic, dyskinetic, and ataxic types. Specifically, areas of sensorimotor functioning, language and verbal skills, visual-spatial and perceptual skills, learning and memory, and executive functioning are reviewed. Implications for learning as well as a neurobiological cause of executive function deficits are discussed. Keywords Cerebral palsy . Neuropsychological function . Spastic cerebral palsy . Dyskinetic cerebral palsy . Ataxic cerebral palsy . Pediatric cerebral palsy . Neuropsychological function in cerebral palsy . Subtypes of cerebral palsy Cerebral palsy (CP) has been defined as a term that describes a group of disorders of movement and posture, which limits activity and results from brain injury before development of the brain is complete (Bax et al 2005; Krigger 2006). CP is considered non-progressive in that the primary lesion, anomaly, or injury remains static; however, the clinical appearance may change due to growth of the central nervous system (Sankar and Mundkur 2005). CP is primarily associated with a wide variety of motor disruptions as well as associated disruptions (Bax et al. 2005). In some cases, symptoms associated with CP can intensely hinder normal activities of everyday life. Often, children with CP experience associated disabilities, such as cognitive impairments, epilepsy, abnormal growth, sensation abnormalities, vision problems, and hearing problems (Cheney & Palmer 1997; Krigger 2006). Feeding problems, gastroenterological problems, and incontinence are also associated
K. Straub : J. E. Obrzut (*) Department of Special Education, Rehabilitation and School Psychology, College of Education, The University of Arizona, Tucson, AZ 85721-0069, USA e-mail: jobrzut@u.arizona.edu

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symptoms in some children with CP. Additionally, children with CP are also five times more likely to experience behavior problems (Odding et al. 2006). Speech and language problems related to either poor muscle control or cognitive impairments have also been demonstrated by children with CP (Sankar and Mundkur 2005). It is also of interest to consider specifically neuropsychological and cognitive functioning in children with CP. A previous review by Fennell and Dikel (2001) indicates a dearth of information in this domain; although in recent years, neuropsychological studies and use of medical technology continue to advance, and have led to a better understanding of functioning in children with CP. Research findings on the neuropsychological and cognitive functioning of children with CP are reviewed and suggests a neurobiological cause for at least one of these effects; however, a description of CP types and associated brain damage is first presented.

Types of CP There is wide variation in the manifestations of cerebral palsy and classification of CP types is made based on the primary motor deficits (Fennell and Dikel 2001). In addition to primary motor deficits, children with CP manifest associated symptoms. Depending on the clinical presentation, children with CP are classified into one of four types. Mixed CP is diagnosed when no primary movement disorder is observed (Pueyo et al. 2003). The spastic CP type is characterized by increased deep tendon reflexes, tremors, increased muscle tone, muscle weakness, and gait disturbances. It has been suggested that spastic CP dominates the majority of cases, with prevalence rates of approximately 7077% (Sankar and Mundkur 2005; Yeargin-Allsopp et al. 2008). Within the spastic type there are three subtypes, which are distinguished according to the affected area of the body. Quadriplegia spastic CP includes spasticity and stiffness can affect both arms and legs and is the most severe form of CP. Within this quadriplegia spastic CP, voluntary movements are few and swallowing and speaking is difficult. Intellectual deficits are most common in this type. Diplegia spastic CP, a second subtype, involves spasticity occurring primarily in the legs and lower part of the body. The hands may be clumsy and tightness in the legs may produce a scissor gait. The third subtype is hemiplegia spastic CP, which affects the arm and leg on only one side of the body. Children with this subtype might demonstrate tip toeing due to tight heel tendons. Another type is dyskinetic CP, which affects approximately 1015% of children with CP, is characterized by uncontrolled, slow, and writhing movements. Drooling and grimacing are sometimes observed. Ataxic CP, a third main CP type, is present in approximately 5% cases is ataxic CP. In ataxic CP, poor coordination and balance problems are observed. Children with this subtype also experience gait and fine motor problems (Sankar and Mundkur 2005). It is known that all forms of CP are the result of damage to the brain during early fetal development, or just before, during, or just after birth (Bax et al. 2005). There are multiple causes for congenital CP, including intracranial hemorrhage, genetic abnormalities, asphyxia, low birth weight, premature birth, or birth trauma (Krigger 2006). Conversely, acquired CP is the result of damage to the brain in the first few months or years of life. There are also several possible causes of postnatal damage,

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such as brain infections (bacterial meningitis or viral encephalitis), accidental head injury, or child abuse. There are a variety of risk factors for having CP, and in many cases a full understanding of the cause is unclear. Although there have been advancements in understanding etiology, prevention, and treatment of CP, the prevalence of CP has not decreased in recent years (Cheney and Palmer 1997). In fact, the prevalence of CP has increased to over two per 1000 live births (Odding et al. 2006). Medical advances in obstetrics and prenatal and postnatal care may be related to the increasing rates of CP. Advancements leading to increased survival rates of premature infants and low birth weight infants coupled with continued or increased rates of impairment have contributed to the rising number of children with CP (Hoon 2005). Although cause of injury can vary, research has identified four main types of brain damage, which can result in CP. Neuroimaging techniques such as Magnetic Resonance Imaging (MRI) and Head Computer Tomography (CT) have been utilized for studying types and location of damage, which are then interpreted along with the clinical phenotypes of CP (Bax et al. 2006; Hoon 2005). Some studies have revealed a high rate of abnormal MRI scans in children with CP (Bax et al. 2006; Krgeloh-Mann and Horber 2007; Yin et al. 2000). These MRI scanning techniques has identified several types of brain damage. Specifically, one type of abnormality is damage to the white matter of the brain that results in periventricular leukomalacia (PVL). Such damage results in thinning of the posterior body of the corpus callosum, enlargement of the lateral ventricles, and irregularity of the lateral ventricular walls (Melherm et al. 2000). This type of damage occurs early in gestation, when the white matter is most vulnerable (Hoon 2005). Second, abnormal brain development or cerebral dysgenesis can occur. This type of damage refers to any disruption of normal brain growth during fetal development where malformations can interfere with brain signal delivery. A third type of damage is intracranial hemorrhage or bleeding in the brain and is caused by faulty blood vessels. In some cases, the fetus suffers a stroke due to blocked blood flow. Additionally, brain damage caused by lack of oxygen or asphyxia is a fourth type of abnormality that can cause CP. Asphyxia in infancy is also sometimes known as hypoxiischemic encepholopathy, a condition that destroys tissue in the cerebral motor cortex and other areas of the brain, such as the basal ganglia or thalamus (Wu et al. 2006). Patterns of brain injury in patients with CP are very much related to the gestational age of occurrence (Yin et al. 2000). For instance, the fetal brain is most vulnerable for PVL damage between 28 and 34 weeks, whereas after 34 weeks, subcortical and cortical regions are the more vulnerable for hypoxic-ischemic injury (Hoon 2005). In a study on 585 children with CP, Bax et al. (2006) found that PVL was the most prevalent type of damage (42.5%), followed by basal ganglia lesions (12.8%), cortical/ subcortial lesions (9.4%), brain malformations (9.1%), focal infarcts (7.4%), and miscellaneous lesions (7.1%). It should be noted that the majority (79.1%) of participants in this study had spastic CP, although Bax et al. (2006) more specifically delineates the findings of each type of damage related to the subtypes. The correlation between types of brain damage to clinical classifications is not completely clear. Krgeloh-Mann and Horber (2007) analyzed MRI findings from various studies according to CP types. In diplegia spastic CP or quadriplegia spastic CP, periventricular white matter lesions were found in 63%, brain abnormalities were

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found in 9%, and cortical or deep gray matter lesions were observed in 13% of CP patients. For patients with hemiplegia spastic CP, periventricular white matter damage occurred in 36%, brain abnormalities occurred in 16%, cortical or deep gray matter lesions occurred in 31%, and 7% had miscellaneous lesions. There were few data provided for the dyskinetic CP type. However, cortical or deep gray matter lesions occurred more often than PVL damage. In reviewing research, Cheney and Palmer (1997) and Krgeloh-Mann and Horber (2007) indicated that damage to the motor cortex account for clinical aspects of spastic CP, where as basal ganglia or thalamus damage account for dyskinetic symptoms. According to Krgeloh-Mann and Horber (2007), acquired or injuries of lesional origin generally account for the spastic and dyskinetic types. In addition, the authors also noted in their study that children with ataxic CP showed fewer incidences of abnormal brain scans and these images were not often clearly lesional in nature. It is clear that there is considerable variety in clinical presentation, as well as with the cause and nature of brain damage in children with CP. As such, the neuropsychological and cognitive research findings are reviewed in the areas of sensorimotor functioning, language and verbal skills, visual-spatial perceptual skills, learning and memory, and executive functioning on children with a CP diagnosis, including the spastic, dyskinetic, and ataxic types.

Motor Functioning In accordance with the fact that impaired coordination of muscles and movement is the defining characteristic of a diagnosis of CP, children with CP demonstrate clinical deficits on assessments of gross and fine motor function. One study found that children with CP demonstrated variable fine and gross motor skills, ranging from significantly low to near normal ranges of function (Vohr et al. 2005). Children with spastic quadriplegia CP were the exception, as this group is typically more often severely impaired. According to Reddihough (2006), the Gross Motor Function Classification System (GMFCS) and the more recently developed Manual Ability Classification System (MACS) are two common measurement tools used among researchers and clinicians. For example, Himmelmann et al. (2006) utilized the GMFCS as a measure of gross motor function and found that 70% of CP children functioned with mild to moderate gross motor impairments and 30% functioned with more severely impaired gross motor functions. In a similar pattern, 74.5% of children with CP exhibited mild to moderate fine motor impairments and 25.5% demonstrated more severely impaired fine motor impairments. Both gross motor and fine motor impairments differed significantly between CP type, illustrating wide-ranging manifestations of symptoms of CP. Gross motor impairments were also strongly correlated with at least three associated impairments such as visual impairments, learning disabilities, and epilepsy. This suggests that gross motor impairments provide an indication of the childs overall disabling condition in those diagnosed with CP. In understanding motor related difficulties in cerebral palsied children, van der Weel et al. (1996) suggested that both perceptual variables and motor variables must be analyzed in light of the fact that the perceptual information the child gleans from

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the environment guides coordination of movement of the body part to a certain location. Furthermore, in review of their previous work on cerebral palsied children and movement, van der Weel et al. (1996) concluded that children with CP have more difficulty with motor tasks that do not provide them with adequate sensory information. In one such study, children with CP showed significantly better range of motion banging a drum than performing the same action without the drum and stick. These findings suggested that ample environmental sensory information should be provided to the CP child in order to facilitate perceptual-motor learning and rehabilitation. In terms of more specific impairments, children with spastic CP have shown deficits in visual motor precision and figure reproduction, indicative of difficulties with fine motor skills (Dellatolas et al. 2005; Pirila et al. 2004). Fine motor hand limitations that children with spastic CP experience appear to be related to neuropsychological outcomes. For example, Dellatolas et al. (2005) examined quality of hand skill and neuropsychological outcomes of a group of children with spastic CP without mental retardation compared to a control group with no disabilities. Hand function was measured by a Computerized Peg Moving Task, in which participants were required to move each of ten pegs, one by one, to the hole in an opposite row. For each case of the participants right, left, best, and worst hand, the control group performed significantly better than the CP participants. More specifically, results showed that 30% of children with hemiplegia spastic CP showed impairment of the unaffected hand and 70% of children with diplegia showed impairment of both hands. Additionally, degree of hand impairment in the right hand was associated with phonological and meta-phonological skills and impairment in the left hand was associated with visual-spatial and counting abilities on a comprehensive neuropsychological battery. Results revealed that hand impairment was not associated with reading but was with phonological deficits, leading the authors to suggest that oral-motor difficulties such as articulation and speech production impairments might account for these phonological deficits. Slower articulation rates in children with CP have been observed elsewhere in the literature (White et al. 1994). Thus, it appears likely that in CP patients, the degree of hand skill deficit is a more important factor in specific neuropsychological outcomes than is left hand/right hand asymmetry in hand function. Given the above findings, it may be concluded that motor limitations are the mark of CP and children with CP demonstrate a wide range of gross and fine motor abilities. Specifically, perceptual deficits have been shown to influence motor precision, as adequate sensory information from the environment is necessary to facilitate movement and motor skills. CP children have also shown difficulties in visual motor and fine motor skills. Hand skill in particular appears to be related to other deficits such in phonological skills, which may also be influenced by possible motor limitations on articulation skills.

Language and Verbal Abilities Children with CP often demonstrate difficulties in communication and language use. Capacity for language use typically depends on the level of motor, intellectual, or

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sensory impairments. However, basic linguistic abilities are often comparable to control groups as noted by Sabbadini et al. (2001). Several studies have also demonstrated average verbal abilities of higher functioning CP children and furthermore, some studies reveal better verbal abilities than nonverbal abilities as measured by intelligence tests (Carlsson et al. 1994; Pirila et al. 2004; Sabbadini et al. 2001; White and Christ 2005). In addition, children who experience hemiplegic spastic CP on the right side (with early left hemispheric brain lesions) have demonstrated spared language skills. According to Lidzba et al. (2006), in right hemiplegic spastic CP patients, language reorganizes to the right side of the brain, and is possibly influential in the visual perceptual and visual spatial deficits demonstrated by these patients who have injuries on the left side of the brain. Furthermore, it appears that children with more severe CP experience varied difficulties with language. Pirila et al. (2007) found that in a group of children with CP (ages 1, 10 months9, 0 months), the severity of functional motor limitation together with measured intelligence was related to language and motor speech problems. Specifically, children with an IQ above 70 only demonstrated deficits in the motor speech domain (oral-motor skills, phonology, and articulation skills). However, the group did not reveal deficits either in verbal comprehension (passive vocabulary and comprehension of grammatical structures) or verbal expression (naming, similarities, and grammatical skills). On the other hand, children with an IQ lower than 70 demonstrated impairments in verbal expression, comprehension, and motor speech skills. Furthermore, none of the children with IQs above 70 met criteria for a specific language disorder, whereas children with IQs below 70 exhibited more pervasive language and speech impairments. It was also found that the more severe the CP in terms of gross and motor impairments, the more speech and language problems were present. Lastly, neonatal (cranial) ultrasounds taken at birth correlated with motor skills but were not predictive of higher order cognitive functions. Other data also demonstrate how severe CP can affect language skills, that is, when children with CP experience motor difficulties that inhibit speech ability (dysarthria or anarthria). Dahlgren-Sandberg and Hjelmquick (1997) investigated language skills of nonvocal cerebral palsied children, compared to two vocal groups, one matched for mental age and gender and the other matched for mental age and chronological age. The nonvocal CP children all utilized the Bliss symbol system of communication along with hand signals. The participants were assessed for phonemic awareness, verbal memory, verbal comprehension, reading, and spelling. Results revealed that nonvocal cerebral palsied children appear to have impaired reading, spelling, and verbal comprehension skills when compared to controls. Phonemic awareness skills were not significantly different than either control group. Reading skills were impaired, however, suggesting that as opposed to basic phonemic awareness, more complex skills needed for reading were impaired, such as mental manipulation on the phonemic level and recoding. Similarly, Card and Dodd (2006) found that compared to vocal CP children, non vocal CP children were impaired in phonological awareness skills that require more mental processing, such as written rhyme judgment, syllable segmentation, and phoneme manipulation. There were no differences between the groups with more basic phonological skills such as identification of syllables, reading non-words, and judging spoken rhyme.

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Additionally, in the Dahlgren-Sandberg and Hjelmquist (1997) study, a within group analysis showed that the use of synthetic speech aided in better performances in reading and spelling, thereby highlighting the importance of acoustic rehearsal in facilitating the acquisition of language skills in children with CP who have oral motor limitations. Similar to this role of acoustic rehearsal in developing verbal skills, auditory perception skills have been shown to be related to spelling and reading in some children with CP. Earlier, Dorman et al. (1984) examined 25 adolescents with severe forms of CP. There were a range of IQ scores from 50 to 103. Findings showed that the Rhythm factor and perception of rapid auditory stimuli were highly predictive of reading and spelling skills. These results highlight the importance of auditory perception in acquiring academic skills, particularly in reading. Further, in a sample of 31 adolescents with varying types of CP, Dorman (1987) investigated whether measures of verbal production, speech perception, nonverbal auditory perception, and visual-spatial skills from the Luria-Nebraska Neuropsychological Test Battery, in addition to Verbal IQ (VIQ), were associated with reading scores. Visuospatial organization was the most impaired neuropsychological skill, although it was not associated with reading skills. Reading comprehension was also impaired among all subtypes of CP, whereas reading recognition was intact relative to the respective VIQ in diplegic and hemiplegic participants. Thus, although nonverbal auditory perception and VIQ were most highly correlated with reading skills, out of the two, nonverbal auditory perception was more highly correlated with reading skills. Both skill areas were also related to reading comprehension. Taken together, these studies reveal that sensory deficits such as auditory impairments may be related to language skills in children with CP, particularly in reading and spelling. Overall, language use and verbal abilities appear to vary in patients with CP according to their level of impairment. In general, verbal abilities have been shown to be more developed than nonverbal abilities in children with less severe CP. However, children with more severe CP, including associated deficits such as IQ below 70 and dysarthria or anarthria, show greater deficits in verbal and language abilities when compared to children without these associated impairments.

Visual-Perceptual and Visual Spatial Abilities Studies have revealed that children with CP also demonstrate deficits in visual perceptual abilities and visual spatial abilities (Dellatolas et al. 2005; Kozeis et al. 2007; Sabbadini et al. 2001). One such area of deficit may be visual proprioceptive mapping ability in children with CP. For example, Wann (1991) found that proprioceptive function in adolescents with various types of CP was not enhanced by visual cueing, whereas normal participant adults showed an advantage with proprioceptive tasks that were aided by visual cues. Thus, adolescents with CP had difficulties mapping between the visual system and proprioceptive system. Several hypotheses may explain the possible reason for these difficulties. Wann (1991) suggested that a visual bias resulting in impaired visual spatial judgments might be involved. Although no participants revealed problems on an optometric exam, a slight visual bias may exist. Alternatively, adolescents with CP might have cortical

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damage such that a neural structure necessary for mapping between the visual system and the proprioceptive system may be impaired. Lastly, children with CP may experience and develop adaptive skills within an unstable perception-movement system. This explanation is most promising as new adaptive skills could be taught to the child as a rehabilitation method. Several other studies have shown that visual perceptual deficits are related to many areas of function in children with CP. It has been established that children with visual perceptual difficulties have concomitant visual skill deficits that lead to reading difficulties (Kozeis et al 2006). Also, children with spastic diplegia CP who exhibit visual perceptual difficulties also show slower rates in processing visual imagery in contrast to CP and normal control participants without visual perceptual deficits (Courbois et al. 2004). Further, Fedrizzi et al. (1996) showed that children with preterm spastic diplegia CP demonstrated a significant discrepancy between Wechsler scale Verbal IQ and Performance IQ scores, with lower Performance IQ scores, suggestive of deficits in the visual perceptual domain. This studys value is increased due to the fact that PVL damage was evident in the MRI findings of the participants. Specifically, severity of ventricular dilation, the extent of white matter reduction, optic radiator involvement, and thinning of the posterior corpus callosum correlated with Performance IQ. Based on these findings, the authors postulated that PVL damage related to visual input impairments might be involved in the visual perceptual deficits reflected by the Performance IQ. A noted weakness in the literature is that in an effort to delineate the visual perceptual deficits in children with CP, many studies have evaluated these deficits compared to overall intellectual functioning. Considering that children with CP often have deficits in nonverbal intelligence, comparison to overall intelligence may result in an overestimation of visual perceptual deficits. To counter this oversight, Stiers et al. (2002) examined visual perceptual ability of a random sample of CP children and a control group on subtests of nonverbal IQ. The authors selected visual-perceptual tasks that measured visual-constructional ability, perceptual categorization, and visual matching abilities. Results showed that compared to the control group, children with spastic CP demonstrated visual-perceptual impairments and that impaired performance on the tasks were neither related to the level of mental retardation nor to nonverbal intelligence. Therefore, individuals with spastic CP would exhibit deficits in visual-perceptual domains, regardless of IQ level or intelligence domains (verbal vs. nonverbal). In accordance with this, Stiers and Vandenbussche (2004) also concluded that visual perceptual deficits observed in children with CP are independent of nonverbal IQ test scores, which is contrary to previous claims that visual perceptual impairments in children with CP are reflected in nonverbal IQ scores. Although Stiers and Vandenbussche (2004) maintain that these visual perceptual deficits are not specifically related to nonverbal IQ scores, it is probable that both nonverbal IQ impairments and visual perceptual impairments may be served by the same or related neural substrate. Pirila et al. (2004) were interested in relating findings from cranial ultrasounds taken at just after birth on children with spastic diplegia with visual-spatial and visual perceptual task performance on the NEPSY test battery. Although there were no associations found between ultrasound results and the NEPSY results, the children with CP scored significantly poorer than the mean on measures of visual-spatial

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function. Specifically, this group scored lower on the Design Copying, Arrows, and Block Construction subtests. Children with visual impairments also performed significantly poorer on the Design Copying subtest. In addition, imaging results suggested PVL and posterior cortical damage. The authors concluded that cognitive correlates of posterior cortical damage, likely the visual-spatial correlates, were impaired based on the neuropsychological performance. Consistent with previous results, Lidzba et al. (2006) also found visual spatial deficits in a specific group of CP patients with non-epileptic, right side hemiplegic spastic cerebral palsy. Interestingly, language function was intact, despite damage on the left side of the brain suggesting that in these patients, language function reorganizes to the right side of the brain. Thus, it is likely that language reorganization to the right side in hemiplegic spastic CP patients leads to a crowding of the right hemisphere of the brain, leaving less neural substrates available for normal functioning of visual-spatial abilities. These findings, taken together with the findings from studies on visual perception and visual-spatial functions, reveal that this neuropsychological domain is often affected in individuals who experience CP. In many cases, PVL damage and visual skill deficits are likely involved as well.

Learning and Memory Due to the wide-ranging limitations children with CP experience, learning and memory problems frequently occur. For example, stensj et al. (2003) reported that in a sample of children with all CP types, 44% experienced difficulties learning, memorizing, and applying attained knowledge. More recently, Himmelmann et al. (2006) found the incidence of learning disabilities (LD) to vary depending on the clinical type of CP. In hemiplegics, LD occurred at 17%, diplegics at 49%, quadriplegics at 100%, dyskinetic type at 62%, and at 50% in the ataxic type. LD occurred on average in 40% of the sample. Dahlgren-Sandberg (2006), in a longitudinal study, examined literacy learning in a group of nonvocal CP children with severe motor limitations and normal IQ compared to a group of normal control children. While the CP children showed, albeit slow, some development in phonological skills, there were no gains in short-term memory compared to the gains observed in the control group. Furthermore, initial performance of short-term memory was significantly worse than the control group. Another primary result was that the children with CP had difficulty acquiring reading and spelling skills, where normal intelligence and phonological gains would have predicted otherwise. The researchers suggested that the deficits in short-term memory might have influenced difficulty in acquiring reading and spelling skills also. Given these findings, the need to examine the role of working memory and the articulatory loop in literacy and skill acquisition for children with CP is warranted. White et al. (1994) investigated the role of articulation rates in working memory with children suffering from spastic diplegic CP because participants with CP have demonstrated slower articulation rates compared to control participants. White et al. (1994) hypothesized working memory performance would also be impaired, based on the notion that subvocal articulatory loop underlies working memory performance. However, contrary to the hypothesis, working memory for auditorily presented verbal material in children with CP was found to be commensurate with that of the control

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group. The authors postulated that either normal, overt articulation rates are not necessary for working memory performance or the children with spastic diplegia CP generated alternative memory strategies. White et al. (1994) also suggested that spared components in spastic diplegic CP patients such as the parietal-temporal and basal ganglia may be related to a system that subserves short-term retention and manipulation of verbal information, thus accounting for normal working memory performance. An alternative hypothesis that may explain the sparing of working memory in these patients is neural reorganization. That is, in early development, plasticity of the brain may have permitted other brain structures to compensate for the damage to short-term and working memory structures. Carlsson (1997) examined learning and memory function with a group of CP children who experienced mild to moderate spastic hemiplegia. The CP patients were of average intelligence and had no visual or hearing impairments. The findings revealed that the spastic hemiplegic CP participants exhibited intact long-term memory (recall after 1 h and 24 h) for words and drawings when compared to the control group. However, right hemiplegia impaired (left hemisphere lesions) CP children showed slower acquisition for drawings than the control group, but not for words. This could be explained by the reorganization of verbal material to the right hemisphere thereby interfering with right hemisphere visual-spatial working memory functions. Conversely, Sabbadini et al. (2001) found that when intelligence level was controlled, the CP patients with severe neuromotor and verbal disabilities exhibited intact short-term immediate memory for visual-perceptual data (using immediate recognition of Ravens Matrices) whereas long-term verbal memory (word recognition following five presentations) was lower than for the control group. Although these findings are somewhat contrary, they underscore the heterogeneity within the term cerebral palsy and are likely only applicable to the specific nature of the CP and the measures utilized in the study. White and Christ (2005) also investigated short and long term memory with quadriplegic spastic CP children using word lists from the California Verbal Learning Test-Childrens Version. Results revealed that the CP group had more difficulty learning words over five trials, thus reflecting deficits in learning and short-term memory. However, long-term memory performance was comparable to that of the control group. It was also concluded that the medial temporal brain regions that are often involved in associative memory abilities were spared, as evidenced by intact immediate free recall on only the first trial. Further, Schatz et al. (1997) found that children with spastic diplegic cerebral palsy demonstrated deficits in learning paired associates involving visual nonverbal responses, regardless of stimulus type (verbal or nonverbal). Thus, similar to White and Christ (2005), Shatz et al. (1997) discovered deficits related to learning and short-term memory; however, learning difficulties were more specific to items that required a visual, nonverbal response. Lesion severity was also related to the performance requiring the visual, nonverbal response modality. These findings support the general conclusion that verbal abilities in children with CP tend to be more developed than nonverbal abilities. From the studies reviewed, it appears that many children with CP experience variable learning problems. Some individuals with CP have difficulties in short-term and/or long-term memory and are slower learners than the average individual.

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Conversely, some children may have intact memory mechanisms for certain stimuli or response modalities and may also demonstrate intact working memory abilities. Results from learning and memory studies appear to be mixed and are best understood in terms of each subtype of CP and nature of the brain injury.

Executive Functioning and Attention It has been hypothesized that in individuals with CP, higher order executive abilities might be impaired due to damage to the white matter tracts, which connect the prefrontal and posterior brain regions (Christ et al. 2003). For example, a study by White and Christ (2005) suggested deficits in executive functioning in children with quadriplegic spastic CP. Specifically, it was found that the quadriplegic CP participants demonstrated less evidence of a clustering strategy in recalling a list of words when compared to the performance of the control group. These results suggest prefrontal lobe dysfunction, which is the result of PVL damage. Additionally, younger children in the group with CP also had more intrusion errors in recognition memory tasks than younger children in the control group or any of the older participants in either group. This finding suggests a developmental delay and/or deficit for the younger children with CP in executive functioning. Accordingly, Christ et al. (2003) examined inhibitory control in children with bilateral spastic CP. Three measures of inhibitory control were administered to 13 children with bilateral spastic CP and 20 control children. The measures were diverse and included the Stroop Color and Word Test, in which children were required to respond appropriately to presented colored words; a stimulus-response task, in which children were required to respond to peripheral circles on a computer; and an Antisaccade task, in which the participants eye movements towards a stimulus were recorded. Analysis of reaction time (RT) and error data revealed that when age was co-varied out, children with bilateral spastic CP demonstrated deficits in inhibitory control. Specifically, the CP group showed slower RT and more errors than the control group. Upon considering these results, it appears that processing speed (RT) also contributed to the difference between the groups; however, when RT was controlled, the children with CP performed poorer yet than the control group on the Stroop and Antisaccade tasks. These findings demonstrate that, although processing speed may have influenced the overall performance between groups, inhibitory control is likely impaired beyond the effect of slower processing speed in children with CP. The error data, showing more errors for the children with CP also lend support to the deficits observed in inhibitory control. Schatz et al. (2001) examined inhibition of return (IOR), which they describe as an attentional bias that is demonstrated by first drawing attention away from an original location. An attentional bias is then reflected when a person looks faster at a novel location than when switching attention back to the original location. Participants in this study included a group of 39 healthy control participants and 33 children with diplegic spastic CP, which were categorized based on location of brain lesion. A visual orientating task (cue) was used in which the child was required to watch peripheral boxes flash and then respond as quickly as possible with their dominant hand when a bright target star appeared in one of the boxes.

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Two sets of trials were administered; short delay and long delay trials. For each trial, one of the peripheral boxes was cued. The star appeared after a short delay following the cue (50- or 150- ms) in which on 80% of the trials, the star appeared in the cued box and on the remaining 20% of the trials the star appeared in the non-cued box. The long delay trials (600s- or 1000- ms) involved an additionally cued central box after the peripheral cue was elicited but before the target star appeared at random in either peripheral box. These long delay trials specifically tested the IOR mechanism. Results showed that the group with CP who had brain lesions anterior to the central sulcus exhibited impaired function with the IOR mechanism, when compared to the other groups with CP who had damage to a different location and the control group. This may indicate that cerebral palsied children with lesions that disrupt the frontal regions, specifically the frontal-collicular pathways, demonstrate difficulties with inhibition of control. The authors implied that elementary attentional mechanisms such as IOR might be related to higher order cognitive abilities, such as visual functions involved in reading and scanning. Furthermore, these data suggest that deficits in the IOR attentional mechanism are identifiable by the age of six months. Other researchers also support the findings of deficits in executive functioning with individuals who experience CP. For example, impairments measuring visual attention, auditory attention, planning, response time, and inhibition have been cited (Carlsson 1997; Laraway 1985; Pirila et al. 2004). In general, therefore, the literature suggests that children with spastic CP, although ultimately dependent on the particular location of brain injury, may demonstrate deficits on prefrontally or frontally mediated measures of attention and inhibition. Given these findings it is likely that there are some circumscribed set of neurobiological causes for executive function deficits that are unique to individuals with CP discussed below.

Conclusion Cerebral palsy (CP) is a disability caused by early brain lesions and affects coordination of muscle and motor movement. CP is classified by presentation of motor impairments throughout the body. Symptomatic presentation of motor difficulties range from mild to severe and are usually accompanied by associated symptoms which also affect normal functioning. Associated problems may include cognitive impairments, sensory problems, visual problems, and speech and language impairments. The literature delineating neurocognitive and neuropsychological impairments in children with CP is diverse, given the diversity in the nature of brain injury, and presentation of motor and associated symptoms. In considering the pervasive effects of CP on a childs life, the body of literature on the neuropsychological effects of the disorder is not as robust as one might believe. It should be noted that the neuropsychological findings are most relevant to the type most commonly discussed in the literature, the spastic CP type; however, some general conclusions can be made. Motor functioning in children with CP can be less impaired or more severely impaired and is related to the extent of their brain injury. Perceptual deficits account for some of the motor impairments exhibited by children with CP. In particular, left and right hand skill impairments are associated with related hemispheric neuropsychological outcomes. In the higher functioning CP

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children, verbal abilities are superior to nonverbal abilities. However, in more severe cases of CP, verbal and language skills can be impaired, and are often influenced by articulation problems. In terms of nonverbal, visual perceptual, and visual spatial domains, children with CP typically demonstrate deficits. Lower visual skill and PVL damage have also been associated with visual perceptual and visual spatial difficulties. Learning problems occur in about half of the children with CP and it is likely that several factors account for the variation in learning processes. Short-term memory problems and slower learning over repeated trials has been demonstrated. However, long-term memory and immediate memory functions are not as clearly affected. Executive functioning has also shown to be impaired in children with CP. Difficulties with strategy generation, slower response time, more intrusions, and inhibition and attention difficulties have been reported. Deficits in executive functioning are foremost apparent in CP patients who have damage to the prefrontal cortex and disruption of the frontal-collicular pathways, often due to PVL, or white matter damage. Finally, from our perspective, it is apparent that there are numerous neuropsychological manifestations associated with CP in children. Thus, it is likely that there are some circumscribed set of neurobiological causes underlying this condition. For example, Bax et al. (2006) identified white matter abnormalities in 42.5% of their population. It may benefit the field to try to identify, for example, executive function deficits that are peculiar to individuals with CP. These deficits may be correlated with white matter disease, consistent with what is known about basal ganglia structures that mediate executive function deficits. Based on these summarized results, it is clear that children with CP experience functional difficulties in several domains. It would be beneficial to utilize findings from neuropsychological assessments to guide rehabilitation programs. Integration of these results would also be useful in the school setting, as target areas of deficit could be identified for intervention. An intervention would also include a careful assessment of each child and his or her particular type of CP and associated difficulties. Research on the neuropsychological outcomes of children with CP should continue to expand and lead to a greater understanding of CP and its effects on the functioning of these children.

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