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Psychiatric Complications in Cerebral Palsy
Taliba Foster &Aanmol I. K. Rai &Ronald A. Weller &
Thomas A. Dixon &Elizabeth B. Weller
Published online: 13 March 2010
#Springer Science+Business Media, LLC 2010
Abstract Cerebral palsy (CP) is a disorder of motor and
posture impairment resulting from brain injury prior to
completion of cerebral development. It affects 2 to 3 per
1000 individuals. CP is also associated with sensory,
behavioral, cognitive, and emotional sequelae. Few systematic
studies of psychiatric comorbidities in children and
adolescents with CP have been conducted, as the main
focus of concern has been on the physical disabilities.
This has diverted attention from treatable psychiatric
syndromes. Proper psychiatric evaluation of children
with CP is an important task, as appropriate interventions
can help them reach their full potential and enhance the
quality of their lives and those of their families. We
report the case of an individual with CP with behavioral
and emotional symptoms to illustrate the diagnostic
complexity involved. The case highlights the importance
of engaging in a comprehensive diagnostic psychiatric
evaluation process to assess and suggest treatment
options for accompanying comorbid psychiatric conditions.
Keywords Cerebral palsy .Mood disorders in cerebral
palsy .Organic causes of mood disorders .Psychosis
in cerebral palsy .Psychiatry and cerebral palsy
Introduction
Cerebral palsy (CP) is a disorder of motor impairment
resulting from brain injury prior to the completion of
cerebral development [1]. CP is one of the most common
childhood physical disabilities. It affects 2 to 3 per 1000
individuals [2]. This nonprogressive, but not unchanging,
disorder of movement and posture is a consequence of
lesions or anomalies of the brain arising in the early stages
of its development [3]. The most important risk factors for
CP are low birth weight, intrauterine infections, and
multiple gestations [4]. About 20% to 30% cases have no
known cause [5], but the most common etiology is
periventricular leukomalacia associated with prematurity
[6]. Brain development continues during the first 2 years of
life, and any brain insult during the prenatal, postnatal, or
perinatal period can later result in CP [7].
About 70% to 80% of patients with CP have spastic
clinical features [8] and present with increased deep
tendon reflexes, muscular hypertonicity, and scissor gait.
The athetoid or dyskinetic type of CP occurs in 10% to
20% of CP patients and is characterized by abnormally
slow writhing movements of the extremities [8]. The
rarest form is ataxic CP, which impairs balance and
coordination [8].
T. Foster (*):A. I. K. Rai :T. A. Dixon
Department of Child and Adolescent Psychiatry,
The Children’s Hospital of Philadelphia,
University of Pennsylvania,
3440 Market Street, Suite 200,
Philadelphia, PA 19104, USA
e-mail: dr.foster@alumni.upenn.edu
A. I. K. Rai
e-mail: raia@email.chop.edu
T. A. Dixon
e-mail: dixont@email.chop.edu
R. A. Weller
Department of Psychiatry, University of Pennsylvania,
3600 Market Street, 7th Floor,
Philadelphia, PA 19104, USA
e-mail: weller@email.chop.edu
E. B. Weller
The Children’s Hospital of Philadelphia,
University of Pennsylvania,
Philadelphia, PA, USA
Curr Psychiatry Rep (2010) 12:116–121
DOI 10.1007/s11920-010-0096-8
CP traditionally has been viewed as a disorder of motor
impairment. Thus, treatment focus has been mainly on aspects
of its physical disability. Treatable psychiatric syndromes in
this population have been a neglected area of study. To date,
only a few systematic studies of psychiatric comorbidities in
children and adolescents with CP have been conducted. This
is of concern because children with CP have a higher-than-
expected rate of psychiatric disorders [1].
Psychiatric conditions related to CP include adjustment
disorder, personality disorders, depressive symptoms,
parent–child relational problems, difficulties in temperament,
emotional lability, irritability, impulsiveness, attention
deficits, and limited problem-solving skills [5]. Increased
depressive symptoms are significantly associated with
physical disabilities and family environment [5]. Separation
anxiety, oppositional defiant disorder, and attention deficits
are much more common in children with CP [5]. In addition,
major psychiatric diagnoses (eg, mood disorders) may also
co-occur [5]. Two CP patients with juvenile-onset bipolar
disorder were reported by Craven et al. [9].
The difficulties encountered by mental health clinicians
in diagnosing and treating children and adolescents with CP
cannot be understated. To provide information regarding
the psychiatric complications associated with CP, a case of
CP seen at the Mood and Anxiety Disorders Complex
Diagnostic Clinic at the Children’s Hospital of Philadelphia
is discussed.
Patient BG
BG is a 15-year-old female in 10th grade with spastic
diplegia type CP. She was the result of her 33-year-old
mother’s first pregnancy. BG was born at 31.5 weeks by
Caesarian section secondary to premature rupture of
membrane. She weighed 1470 g at birth with an APGAR
score of 5 at birth and 8 at 5 min. She required surfactant
and respiratory support in the neonatal period and remained
in the neonatal intensive care unit for 5 weeks.
BG made good physical progress and had no notable
issues with feeding or sleeping. However, she was
described as having a difficult temperament. At 6 months,
she could not sit up and bear the weight of her head despite
support. Gradually, other motor deficits became evident. By
1 year of age, she was diagnosed with CP, spastic diplegia
type and started on physical and occupational therapy.
BG did not have any speech or social delays and could
communicate verbally with her parents at 18 months of age.
She also underwent eye surgery for strabismus soon
thereafter. A sister was born when she was 21 months
old, and she adjusted well to the sibling. With the help of
occupational and physical therapy, BG walked at 3 years of
age and was toilet trained by 4 years of age.
She started preschool and attended 2 days per week. In
kindergarten, she required an aide to help her secondary to
motor delays. By first grade, she knew she was “different”
and was “left out”of various physical activities at school
and not invited to many social peer events.
Although her strabismus had been surgically corrected,
her visual problems worsened through early and middle
childhood, warranting multiple ophthalmologic consultations.
At 9 years of age, she was diagnosed with retinitis
pigmentosa. She had limited tunnel vision bilaterally
(correctable only to 20/70), decreased visual fields, and
poor depth perception.
BG received multiple physical accommodations in
school but fared well. Her second through seventh grades
at school were “good.”In seventh grade, her classmates did
not want her at the lunch table “because the crutches took
up too much space.”Her transition from a relatively small
middle school to a large and imposing high school in the ninth
grade was anxiety provoking as well as physically and
emotionally difficult. Despite these challenges, she achieved
a grade-point average of 3.694 in 10th grade. However, she
continued to struggle socially, and although she wanted to
have friends, she withdrew from all peers except one.
BG presented to our clinic at 15 years of age with a chief
complaint of “four psychotic episodes”within the past year.
Each “episode”was described as having an acute onset
with sudden remission. She had been assessed by multiple
health providers, and her parents expressed hope that this
evaluation would help them understand the “crazy
episodes.”They also wished to obtain recommendations
that would help their daughter become a successful adult,
especially because she had developed social deficits and
seemed withdrawn.
BG’s first behavioral concerns began 1 year prior to our
evaluation (ie, at age 14 years). At that time, she developed
a sudden change in her sleep pattern. She “stopped
sleeping”and slept for only 2 h in a 36-h period. In the
subsequent 48 h, BG did not show any signs of sleep
deprivation. However, she developed sudden onset of fast
and garbled speech; made paranoid statements (eg, “the
world is after me”); complained of frequent headaches,
body aches, and stomachaches; began talking about “seeing
pink blobs”; and was noted to be laughing hysterically. She
began complaining of feeling very cold, put on three or four
layers of clothing to keep herself warm, and took multiple
hot baths. She started watching Spanish TV channels even
though she did not understand any Spanish and incessantly
repeated phrases and sentences from the shows—as well as
from other people’s conversations—over and over again.
During this episode, she did not display any changes in
level of consciousness; had no hypersexuality, grandiosity,
or any unusually risky behavior; and was oriented to time,
place, person, and situation. She underwent an evaluation at
Curr Psychiatry Rep (2010) 12:116–121 117
her pediatrician’s office, and her vital signs were stable.
Blood tests for antinuclear antibodies and Lyme titers, in
addition to routine blood work, were negative. She was
referred to a neurologist, but no focal neurological deficits
were noted. She underwent a brain MRI and an electroen-
cephalogram (EEG). The EEG was abnormal but was not
consistent with seizure activity, and the changes were thought
to be baseline and secondary to CP. A confirmatory video
EEG was done but was unremarkable for any seizure-like
activity. The brain MRI was also unremarkable.
BG was admitted to a hospital with a diagnosis of acute
change in mental status. She was started on risperidone,
after which her symptoms worsened. Risperidone was
subsequently stopped. Urinalysis and urine culture revealed
a urinary tract infection (UTI). After a course of antibiotics,
symptoms resolved and she returned to baseline. This
sudden behavior change had lasted 25 days.
The second “episode”occurred 19 days later. During this
episode, BG began acting acutely bizarre and was fidgety
and irritable for periods that lasted 20 to 30 min four times
that day. Efforts to calm her down were of no avail. BG
then began to display odd behaviors such as screaming at
her mother, laughing incessantly, and alluding to “being
electrocuted.”Her parents described her as “weird …with
no sense of what was real.”She had insomnia, began to drool
while awake and asleep, and displayed rapid mood shifts. In
the subsequent 48 to 72 h, she developed a fixed gaze in which
her eyes continually drifted down and to the right. A repeat
EEG was performed, and an abnormal spike pattern was
found in the occipital lobes. BG was rehospitalized, at which
point she developed bizarre posturing of her right hand. All
further medical work-up was unremarkable. Her parents were
told that the EEG changes in the occipital lobe and the new
onset of odd behaviors could have been related to a postictal
phase. Repeat EEGs were performed but were negative.
She was started on risperidone as an antipsychotic/mood
stabilizer, lorazepam for agitation and irritability, and
oxcarbazepine plus divalproex sodium for its anticonvulsant/
mood stabilization properties. She responded well to this
regimen and after 17 days returned to her baseline and was
discharged home on risperidone and oxcarbazepine.
Ten days later, the third “episode”occurred. BG again
developed odd behaviors with frequent crying spells. She
talked gibberish in a nonsensical language, rocked back and
forth for hours on end, and again displayed rapid mood
shifts ranging from extreme agitation to becoming morose
and withdrawn. She was assessed at an outpatient clinic,
and divalproex sodium was added to her regimen of
risperidone and oxcarbazepine for mood stabilization. Once
again, she responded and returned to baseline within
10 days of onset of symptoms.
She remained stable and asymptomatic for the next
8 months on these medications. The medications were
gradually tapered, and she remained asymptomatic for
2 months thereafter.
Then, however, she suddenly started acting odd again.
She began reading relentlessly, read out loud for hours,
made references that her food was poisoned, and believed
she was under surveillance. Her speech became bizarre and
“cackling.”Her moods shifted unpredictably and quickly
from being happy to weepy to defiant, irritable, and agitated
within minutes. She would intermittently become limp,
begin drooling, become unable to walk, and needed to be
carried around or required a wheelchair. Soon thereafter,
she had an episode of muscle twitching and developed a
feeling of “being electrocuted.”
This “episode”evolved during a period of 48 h and
warranted her fourth hospital visit, during which she was
diagnosed with postictal psychosis and was restarted on
risperidone. Serial EEGs over the next few days were
unremarkable. A decision was made to do a cerebrospinal
fluid tap.
While awaiting lumbar puncture, she was assessed by a
psychiatrist for the first time. She was diagnosed with
psychotic disorder not otherwise specified. Recommenda-
tions included continuation of risperidone with addition of
divalproex sodium for its mood stabilization and antiseizure
properties.
She underwent another extensive medical work-up that
ruled out thyroid, infectious, or autoimmune etiologies. All
investigations were unremarkable, except for a fungal UTI.
Urology was consulted, and she was successfully treated
for her UTI. She was discharged after 2 days of
hospitalization on divalproex sodium and risperidone.
It was with this past history that she was referred to our
Child and Adolescent Mood and Anxiety Disorders
Complex Diagnostic Clinic for a psychiatric evaluation.
Her spinal tap was scheduled a week after our meeting.
During this evaluation, a family history of attention-deficit/
hyperactivity disorder, obsessive-compulsive disorder,
alcoholism, anxiety, depression, and Asperger’ssyndrome
was obtained. Social history revealed that she lived at home
with her biological parents and 13-year-old brother. She
attended 10th grade at a regular public school, had an
individualized education program that included physical
accommodations as well as a tutor to help her with academics,
and reportedly was a good student. Although she did not
report emotional, behavioral, or learning problems at the time
of the evaluation, parents were concerned about her poor peer
socialization because she had previously been popular at
school with many friends. Current review of systems was
negative except for motor coordination problems related to
CP, poor depth perception related to retinitis pigmentosa, and
recent UTI.
Mental status examination revealed a pretty, petite
15-year-old Caucasian girl who seemed younger than her
118 Curr Psychiatry Rep (2010) 12:116–121
stated age. She was appropriately dressed and groomed and
had an extremely spastic and unstable gait. She needed help
with walking, and when walking unaided, she had difficulty
navigating corners and would often walk into the walls. Her
feet were inverted when sitting, and there was a mild inversion
at the knee joints. Her speech was regular in rate, tone, and
volume with a normal pitch with good clarity and articulation.
She made eye contact but had a blank stare most of the time
and could not track writing on paper. She had a euthymic
mood with congruent and stable affect and displayed
occasional animation of affect when talking about subjects
that interested her. Her thought process was logical and goal
directed, and thought content was appropriate to the current
situation. She was oriented to date, time, place, person, and
situation. She was able to concentrate and completed the serial
sevens test without any errors. She had good registration, as
well as good immediate and 5-min recall without any prompts.
She had a good fund of knowledge and was aware of current
events. She could abstract well. She denied any auditory,
visual, or olfactory hallucinations and stated that her last
visual hallucination was 10 months ago. She denied any
suicidal or homicidal thoughts or any such past thoughts,
plans, or acts. She had good judgment and was insightful
about having medical and social problems.
She was diagnosed as follows:
&Axis I: mood disorder due to (probable) seizure disorder
(rule out bipolar disorder)
&Axis II: none
&Axis III: CP, retinitis pigmentosa, UTI, abnormal EEG
with occipital spikes nonspecific in nature
&Axis IV: growing up with physical and visual handicap,
social isolation at school
&Axis V: Global Assessment of Functioning, 70.
It was recommended that she continue antipsychotic and
anticonvulsant medications for symptom control and mood
stabilization and that future trials of tapering medications be
done under close monitoring of symptoms, preferably by a
child and adolescent psychiatrist.
It was further recommended that she receive individual
interventions that included components of supportive
directive therapy and cognitive-behavioral therapy with a
focus on building independent skills, self-esteem, and
social repertoire. Socialization skills groups and mentoring
programs as a venue for improvement of peer relationships
were also suggested. The role of psychoeducation and
involvement of family members in support groups was
discussed with her parents. It was suggested that school-and
home-based interventions be geared toward maintenance of
daily routines and the earliest possible return to regular
schooling. In terms of her educational environment, it was
decided to review her already-existent individualized
educational program to determine if any changes or new
recommendations/accommodations were needed for the
school.
Discussion
This patient was born premature with a low birth weight.
Prematurity and low birth weight are known risk factors for
CP. Rates of subsequent development of CP are 25 to 31
times higher among infants with a birth weight less than
1500 g compared with full-sized newborn children [5].
Those whose weight is less than 2500 g make up one third
of all infants who later manifest CP [5].
CP usually becomes evident during the period of most
rapid brain growth and is associated with sensory, cognitive,
and behavioral manifestations [5]. Developmental disabilities
associated with CP include mental retardation, sensory
impairment of vision and hearing, learning disabilities,
language disorders, increased prevalence of seizures, cogni-
tive dysfunction, and perceptual disorders, which suggests
that these conditions may have common or related origins
[5]. Thus, CP is not a single entity, and the etiologies of its
multiple presentations are variable. The relative contributions
of prenatal, perinatal, and genetic factors are considered in
determining its etiology [5].
The nature of the illness heavily impacts temperament and
the normal phases of child and adolescent development,
which may interfere with parent-infant attunement [10]. Brain
damage, cognitive impairment, social stigma, and learning
disabilities increase the likelihood of psychiatric disorders
[5]. Brain damage in itself can be a vulnerability factor in the
occurrence of psychiatric disorders [5]. However, it is unclear
whether brain dysfunction leads directly to behavioral
disturbances or causes an increase in the child’s vulnerability
to environmental stress [11].
The extent to which rehabilitation is possible is often
related to the psychological and psychiatric problems that may
coexist with CP [5]. Thus, a psychiatrist or psychologist has
an important role in assessing these children. Although
psychiatric syndromes can be difficult to detect in this
population, any of the following indicates the need for a
comprehensive mental health evaluation:
&Change in personality, such as new onset of sadness,
moodiness, increased irritability, or unusual elation
&Change in appetite, especially if associated with an
increase or decrease in weight
&Change in sleep patterns (eg, excessive sleeping,
difficulty in falling asleep, difficulty in staying asleep,
decreased need for sleep)
&Loss of energy or increased energy levels
&Loss of interest in friends, play, activities, and sports or
absence of pleasure from relationships and activities
Curr Psychiatry Rep (2010) 12:116–121 119
&Low self-esteem, frequently expressed through a negative
view of the self
&Difficulty with concentration
&Feelings of helplessness, occasionally expressed through
suicidal talk
&Aggression and hostility
&Loss of reality testing or hallucinatory phenomena
&Decline in academic achievement.
The psychiatric assessment of a patient with CP should
include an interview with the parents, other caregivers, and
the child. Teacher reports should be obtained whenever
possible. A family history of psychiatric disturbances and
developmental disorders in other family members are
pertinent [5]. Psychological and social factors that affect the
family should be assessed and may include financial stress,
marital stress, frequent absence from work, denial of insurance
or disability benefits, poor caregiver adjustment to the child’s
needs, limited family support, and geographical hardships.
Parents should be evaluated individually to assess how the
child’s illness has impacted their lives, with special focus on
assessing self-blame, depression, projection, dependency, and
substance use [5]. Special considerations during the interview
of the child with CP include accounting for the child’s
developmental and emotional level; determining the most
effective means of communication with the child; and being
patient while relating to a child with a possible speech,
visual, social, or cognitive impediment [5].
The clinical diagnosis should be based on a systematic
developmental timeline review of data. In psychiatric
evaluations of similar cases, objective data can be obtained
using a variety of rating scales in addition to the clinical
interviews. These may include the Children’s Depression
Rating Scale-Revised, Young Mania Rating Scale, Yale-
Brown Obsessive Compulsive Scale, Abnormal Involuntary
Movement Scale, Simpson-Angus Neurological Rating Scale,
Barnes Akathisia Rating Scale, Revised Children’s Manifest
Anxiety Scale (“What I think and feel”), Conners-Wells’
Adolescent Self-Report Scales, Conners’Parent Rating Scale,
Schedule for Affective Disorders and Schizophrenia for
School-Age Children (present and lifetime versions), and the
Children’s Interview for Psychiatric Syndromes (and the
parent’s version).
Parents are active participants in a child’s care and often
function as “co-therapists.”Thus, when they leave the
clinician’s office, they must have a clear understanding of
specific diagnosis and treatment goals. They should feel
hopeful, confident, and well informed about recommendations
[5]. If pharmacotherapy is to be used, the parents and the
child should be actively involved in the decision to use
medication. Parents should be educated about the psychiatric
conditions for which their child is at risk and be given
information regarding advocacy for their special needs child.
In this regard, we have found that imparting information
about the Parents Involved Network and directing families to
http://www.ucp.org,http://www.reachingforthestars.org,and
http://www.thecpnetwork.org are helpful.
Conclusions
Children and adolescents with CP should be regularly
screened by health care providers for mental health issues
with a focus on emotional, behavioral, academic, and social
problems. Care must be taken in assessing and managing
children with CP to ensure that psychological problems are
not overlooked and potentially preventable risk factors are
identified and treated early and effectively [12••]. Family
functioning, physical difficulties, behavioral difficulties,
and motivation are important predictors of social/emotional
adaptation in children with CP [13]. Thus, these factors
should be explored in-depth. Also, the child’s emotional
and developmental age is an important consideration in the
evaluation process, as this may not coincide with the
chronological age. Upon discovery of a psychiatric syndrome,
specific and clear recommendations for intervention should be
made. Treatment may include individual therapy, group
therapy, family work, or medication.
Most importantly, the child with CP and his or her
family should be supported. Using the child’s personal
strength and the family’s strengths in the treatment plan
goes a long way in offering hope, promoting self-esteem,
optimizing the child’s participation in everyday life, and
aiding the family in adapting to their special needs child.
Disclosure Drs. Ronald and Elizabeth Weller are co-owners of the
Children’s Interview for Psychiatric Syndromes (and the parent’s
version) and have received annual royalties from copyright ownership
of this diagnostic interview. Dr. Elizabeth Weller was the principal
investigator for a grant from GlaxoSmithKline to investigate the
tolerability and efficacy of lamotrigine in children and adolescents
diagnosed with bipolar disorder. No other potential conflicts of interest
relevant to this article were reported.
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