Psychiatric Complications in Cerebral Palsy
- First Online:
- Cite this article as:
- Foster, T., Rai, A.I.K., Weller, R.A. et al. Curr Psychiatry Rep (2010) 12: 116. doi:10.1007/s11920-010-0096-8
- 243 Views
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.
KeywordsCerebral palsyMood disorders in cerebral palsyOrganic causes of mood disordersPsychosis in cerebral palsyPsychiatry and cerebral palsy
Cerebral palsy (CP) is a disorder of motor impairment resulting from brain injury prior to the completion of cerebral development . CP is one of the most common childhood physical disabilities. It affects 2 to 3 per 1000 individuals . 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 . The most important risk factors for CP are low birth weight, intrauterine infections, and multiple gestations . About 20% to 30% cases have no known cause , but the most common etiology is periventricular leukomalacia associated with prematurity . 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 .
About 70% to 80% of patients with CP have spastic clinical features  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 . The rarest form is ataxic CP, which impairs balance and coordination .
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 .
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 . Increased depressive symptoms are significantly associated with physical disabilities and family environment . Separation anxiety, oppositional defiant disorder, and attention deficits are much more common in children with CP . In addition, major psychiatric diagnoses (eg, mood disorders) may also co-occur . Two CP patients with juvenile-onset bipolar disorder were reported by Craven et al. .
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.
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 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 electroencephalogram (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. Recommendations 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’s syndrome 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 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.
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.
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 . Those whose weight is less than 2500 g make up one third of all infants who later manifest CP .
CP usually becomes evident during the period of most rapid brain growth and is associated with sensory, cognitive, and behavioral manifestations . Developmental disabilities associated with CP include mental retardation, sensory impairment of vision and hearing, learning disabilities, language disorders, increased prevalence of seizures, cognitive dysfunction, and perceptual disorders, which suggests that these conditions may have common or related origins . 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 .
The nature of the illness heavily impacts temperament and the normal phases of child and adolescent development, which may interfere with parent-infant attunement . Brain damage, cognitive impairment, social stigma, and learning disabilities increase the likelihood of psychiatric disorders . Brain damage in itself can be a vulnerability factor in the occurrence of psychiatric disorders . However, it is unclear whether brain dysfunction leads directly to behavioral disturbances or causes an increase in the child’s vulnerability to environmental stress .
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
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 . 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 . 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 .
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 . 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.
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 . 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.
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.