CASE REPORT
De Novo Cerebral Palsy Diagnosis in 9-Year-Old Soccer Player Presenting With Knee Pain Jérôme Ouellet, MD and Tatiana Jevremovic, MD
Abstract: A 9-year-old boy presented to our outpatient specialized sport and exercise medicine clinic complaining of a subacute onset of unilateral knee pain, after an increased level of soccer training. His knee examination was unremarkable. However, he demonstrated significant tenderness on palpation of his ipsilateral hip flexor and adductor tendons. Abnormalities in muscle tone and difficulty in relaxing and resisting the examiner properly were noted and lead to a complete neurological examination. It demonstrated multiple abnormalities such as increased tone and deep tendon reflexes, greater in lower than upper extremities, and abnormal patterning. A mild form of spastic diplegia was suspected and the patient was referred to a pediatric neurologist who confirmed our initial diagnosis. This case draws attention to the importance of maintaining a high level of suspicion for milder forms of diseases that can go unnoticed for years. Key Words: cerebral palsy, development, pediatrics (Clin J Sport Med 2016;26:e1–e2)
INTRODUCTION Developmental delay in children has many causes, cerebral palsy being one of them. It can affect children to various degrees, making the clinical diagnosis even more challenging. With improved care of pregnant women and premature newborns, an increased number of patients are now presenting to primary care providers.1
CASE REPORT A 9-year-old boy presented with his parents to our outpatient specialized sport medicine clinic, complaining of a traumatic left knee pain. His history was significant only for a new soccer training drill consisting of repetitive kicking using the left leg. He did not complain of mechanical symptoms and did not miss sports. On physical examination, the patient had normal lower extremity alignment. His functional assessment was normal, having difficulties only with performing a single-leg squat. Knee examination was unremarkable. On hip examination, the patient demonstrated exquisite pain over his left hip flexor and adductor tendons. He also had limited hip flexion and extension and pain with resisted Submitted for publication May 28, 2014; accepted November 1, 2014. From the Department of Family Medicine, Western University, London, Ontario, Canada. The authors report no conflicts of interest. Corresponding Author: Tatiana Jevremovic, MD, CCFP (EM), Western University, 3M Building, London, Ontario N6A 3K7, Canada (tjevremovic@ hotmail.com). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Sport Med Volume 26, Number 1, January 2016
hip flexion and adduction. These findings prompted the diagnosis of referred knee pain secondary to hip flexor and adductor tendinitis. Because of increased general tone in his lower extremities and difficulty in relaxing and resisting the examiner properly, a complete neurological examination was conducted. He was alert and oriented throughout the interview. His cranial nerve examination was normal, including fundi evaluation. His tone was increased, more in his lower than upper extremities. Strength and sensation testing were normal. Deep tendon reflexes were symmetrically abnormal: patellar reflexes were 3/4 with spread up to his upper extremities; Achilles reflexes were 2+/4 with spread in his lower extremities; biceps/triceps reflexes were 2+/4 without spread. Spreading is a reflex contraction occurring in a muscle whose tendon was not stretched. His plantar reflexes were normal. His coordination assessment, including gait, balance, and finger-to-nose test, was normal. He, however, demonstrated poor motor planning when trying to transfer from one position to the other, needing some help to secure himself on the examination table. A more thorough assessment of his running pattern could not be performed because of the patient’s symptoms at the time. He was born at 37-week gestation. The pregnancy was significant for macrocephaly, which was followed with multiple ultrasounds. His mother reported using carbamazepine throughout her pregnancy for a seizure disorder. Delivery and perinatal course was unremarkable. At 3 years of age, the patient was assessed by computed tomography scan given the macrocephaly concern and the examination was reported as normal. Growth charts and other past medical records were not available for review. He was also diagnosed with bilateral congenital hearing loss (60%) at 4 years of age and treated with hearing aids. There was a strong maternal familial history of hearing loss: mother’s grandmother, uncles, and cousins being affected. He reached his major motor developmental milestones within normal limits. However, his mother described him as a very clumsy child from the start. He was always falling more than his friends, running slower, and awkwardly. This was never medically investigated. Although he was involved in competitive soccer, his mother stated that he was having a hard time keeping up with his teammates. Neither parent reported school problems. The patient was prescribed compression shorts and was referred to a physiotherapist to address his hip flexor and adductor tendinitis. He was also assessed by a pediatric neurologist, who clinically confirmed our suspicion of mild spastic diplegia. Brain magnetic resonance imaging was unremarkable, without periventricular leukomalacia or white matter lesions (which can be present in more than 70% of cases2). Given the patient’s functional status, he was told by the neurologist to continue with his physiotherapy program and to follow-up with him 6 months later.
DISCUSSION Cerebral palsy (CP) has been defined by an International Workshop as a “group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that www.cjsportmed.com |
e1
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Ouellet and Jevremovic
Clin J Sport Med Volume 26, Number 1, January 2016
FIGURE 1. Motor syndromes of cerebral palsy.5 Figure hosted on www.pathophys.org. Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.
occurred in the developing fetal or infant brain.”3 It is the most common form of chronic motor disability that begins in childhood, affecting 2 to 2.5 per 1000 live births worldwide.2,4 There are various causes associated with CP (genetic, brain malformations, infections, anoxic injuries among others), 80% of which tend to occur before labor and birth. Cerebral palsy is associated with various comorbidities, including cognitive disability, seizures, epilepsy, visual/hearing/cognitive problems, and behavioral abnormalities. Multiple classification systems have been published to try to categorize this disorder, mainly according to function.1 One of the most popular classifications is based on the involved extremities,2 as illustrated in Figure 1. Spastic hemiplegia refers to ipsilateral upper and lower extremity involvement. Spastic diplegia refers to bilateral spasticity of the lower more than the upper extremities. It is often identified by an abnormal crawling pattern (commando crawl). Spastic quadriplegia, the most severe form of CP, affects all 4 extremities. This form is often associated with significant problems such as seizures, cognitive disability, and swallowing difficulties. Extrapyramidal CP, a less common form, is marked by dyskinesia and oropharyngeal difficulties (swallowing and talking). Given the variety of signs and symptoms, clinicians need to keep a high level of suspicion for CP. Levine6 published in 1980 an easy mnemonic describing clinical motor abnormalities that should raise clinical suspicion for CP. He divided them in 6 groups: Postures and movement patterns; Oral motor patterns; Strabismus; Tone of
e2
| www.cjsportmed.com
muscles; Evolution of postural reactions and landmarks; and deep tendon, infantile and plantar Reflexes (POSTER). Abnormalities in 4 or more of these groups significantly increase the likelihood of CP. This clinical case highlights the importance of maintaining a high level of suspicion for such milder forms of diseases usually diagnosed in the first few months of life, but which can go undiagnosed for years. Isolated motor abnormalities are the highlight of the CP spectrum. Increased tone is a risk factor for developing tendinitis, with CP patients often suffering from flexion contractures. Better diagnosis will assist parents and primary care providers in providing care and focused help to these children. REFERENCES 1. Rethlefsen SA, Ryan DD, Kay RM. Classification systems in cerebral palsy. Orthop Clin North Am. 2010;41:457–467. 2. Johnston MV. Cerebral palsy. In: Kliegman RM, Stanton BF, Schor NF, et al, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier; 2011:2061–2065. 3. Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl. 2007;109:8–14. 4. Ashwal S, Russman BS, Blasco PA, et al. Practice parameter: diagnostic assessment of the child with cerebral palsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2004;62:851–863. 5. Rogers L, Wong E. Cerebral palsy. McMaster Pathophysiology Review. 1st ed. 2013. Web site. http://www.pathophys.org/cerebralpalsy/. Accessed May 21, 2014. 6. Levine MS. Cerebral palsy diagnosis in children over age 1 year: standard criteria. Arch Phys Med Rehabil. 1980;61:385–389.
Copyright Ó 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
De Novo Cerebral Palsy Diagnosis in 9-Year-Old Soccer Player Presenting With Knee Pain Jérôme Ouellet, MD and Tatiana Jevremovic, MD
Abstract: A 9-year-old boy presented to our outpatient specialized sport and exercise medicine clinic complaining of a subacute onset of unilateral knee pain, after an increased level of soccer training. His knee examination was unremarkable. However, he demonstrated significant tenderness on palpation of his ipsilateral hip flexor and adductor tendons. Abnormalities in muscle tone and difficulty in relaxing and resisting the examiner properly were noted and lead to a complete neurological examination. It demonstrated multiple abnormalities such as increased tone and deep tendon reflexes, greater in lower than upper extremities, and abnormal patterning. A mild form of spastic diplegia was suspected and the patient was referred to a pediatric neurologist who confirmed our initial diagnosis. This case draws attention to the importance of maintaining a high level of suspicion for milder forms of diseases that can go unnoticed for years. Key Words: cerebral palsy, development, pediatrics (Clin J Sport Med 2016;26:e1–e2)
INTRODUCTION Developmental delay in children has many causes, cerebral palsy being one of them. It can affect children to various degrees, making the clinical diagnosis even more challenging. With improved care of pregnant women and premature newborns, an increased number of patients are now presenting to primary care providers.1
CASE REPORT A 9-year-old boy presented with his parents to our outpatient specialized sport medicine clinic, complaining of a traumatic left knee pain. His history was significant only for a new soccer training drill consisting of repetitive kicking using the left leg. He did not complain of mechanical symptoms and did not miss sports. On physical examination, the patient had normal lower extremity alignment. His functional assessment was normal, having difficulties only with performing a single-leg squat. Knee examination was unremarkable. On hip examination, the patient demonstrated exquisite pain over his left hip flexor and adductor tendons. He also had limited hip flexion and extension and pain with resisted Submitted for publication May 28, 2014; accepted November 1, 2014. From the Department of Family Medicine, Western University, London, Ontario, Canada. The authors report no conflicts of interest. Corresponding Author: Tatiana Jevremovic, MD, CCFP (EM), Western University, 3M Building, London, Ontario N6A 3K7, Canada (tjevremovic@ hotmail.com). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Sport Med Volume 26, Number 1, January 2016
hip flexion and adduction. These findings prompted the diagnosis of referred knee pain secondary to hip flexor and adductor tendinitis. Because of increased general tone in his lower extremities and difficulty in relaxing and resisting the examiner properly, a complete neurological examination was conducted. He was alert and oriented throughout the interview. His cranial nerve examination was normal, including fundi evaluation. His tone was increased, more in his lower than upper extremities. Strength and sensation testing were normal. Deep tendon reflexes were symmetrically abnormal: patellar reflexes were 3/4 with spread up to his upper extremities; Achilles reflexes were 2+/4 with spread in his lower extremities; biceps/triceps reflexes were 2+/4 without spread. Spreading is a reflex contraction occurring in a muscle whose tendon was not stretched. His plantar reflexes were normal. His coordination assessment, including gait, balance, and finger-to-nose test, was normal. He, however, demonstrated poor motor planning when trying to transfer from one position to the other, needing some help to secure himself on the examination table. A more thorough assessment of his running pattern could not be performed because of the patient’s symptoms at the time. He was born at 37-week gestation. The pregnancy was significant for macrocephaly, which was followed with multiple ultrasounds. His mother reported using carbamazepine throughout her pregnancy for a seizure disorder. Delivery and perinatal course was unremarkable. At 3 years of age, the patient was assessed by computed tomography scan given the macrocephaly concern and the examination was reported as normal. Growth charts and other past medical records were not available for review. He was also diagnosed with bilateral congenital hearing loss (60%) at 4 years of age and treated with hearing aids. There was a strong maternal familial history of hearing loss: mother’s grandmother, uncles, and cousins being affected. He reached his major motor developmental milestones within normal limits. However, his mother described him as a very clumsy child from the start. He was always falling more than his friends, running slower, and awkwardly. This was never medically investigated. Although he was involved in competitive soccer, his mother stated that he was having a hard time keeping up with his teammates. Neither parent reported school problems. The patient was prescribed compression shorts and was referred to a physiotherapist to address his hip flexor and adductor tendinitis. He was also assessed by a pediatric neurologist, who clinically confirmed our suspicion of mild spastic diplegia. Brain magnetic resonance imaging was unremarkable, without periventricular leukomalacia or white matter lesions (which can be present in more than 70% of cases2). Given the patient’s functional status, he was told by the neurologist to continue with his physiotherapy program and to follow-up with him 6 months later.
DISCUSSION Cerebral palsy (CP) has been defined by an International Workshop as a “group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that www.cjsportmed.com |
e1
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Ouellet and Jevremovic
Clin J Sport Med Volume 26, Number 1, January 2016
FIGURE 1. Motor syndromes of cerebral palsy.5 Figure hosted on www.pathophys.org. Adaptations are themselves works protected by copyright. So in order to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.
occurred in the developing fetal or infant brain.”3 It is the most common form of chronic motor disability that begins in childhood, affecting 2 to 2.5 per 1000 live births worldwide.2,4 There are various causes associated with CP (genetic, brain malformations, infections, anoxic injuries among others), 80% of which tend to occur before labor and birth. Cerebral palsy is associated with various comorbidities, including cognitive disability, seizures, epilepsy, visual/hearing/cognitive problems, and behavioral abnormalities. Multiple classification systems have been published to try to categorize this disorder, mainly according to function.1 One of the most popular classifications is based on the involved extremities,2 as illustrated in Figure 1. Spastic hemiplegia refers to ipsilateral upper and lower extremity involvement. Spastic diplegia refers to bilateral spasticity of the lower more than the upper extremities. It is often identified by an abnormal crawling pattern (commando crawl). Spastic quadriplegia, the most severe form of CP, affects all 4 extremities. This form is often associated with significant problems such as seizures, cognitive disability, and swallowing difficulties. Extrapyramidal CP, a less common form, is marked by dyskinesia and oropharyngeal difficulties (swallowing and talking). Given the variety of signs and symptoms, clinicians need to keep a high level of suspicion for CP. Levine6 published in 1980 an easy mnemonic describing clinical motor abnormalities that should raise clinical suspicion for CP. He divided them in 6 groups: Postures and movement patterns; Oral motor patterns; Strabismus; Tone of
e2
| www.cjsportmed.com
muscles; Evolution of postural reactions and landmarks; and deep tendon, infantile and plantar Reflexes (POSTER). Abnormalities in 4 or more of these groups significantly increase the likelihood of CP. This clinical case highlights the importance of maintaining a high level of suspicion for such milder forms of diseases usually diagnosed in the first few months of life, but which can go undiagnosed for years. Isolated motor abnormalities are the highlight of the CP spectrum. Increased tone is a risk factor for developing tendinitis, with CP patients often suffering from flexion contractures. Better diagnosis will assist parents and primary care providers in providing care and focused help to these children. REFERENCES 1. Rethlefsen SA, Ryan DD, Kay RM. Classification systems in cerebral palsy. Orthop Clin North Am. 2010;41:457–467. 2. Johnston MV. Cerebral palsy. In: Kliegman RM, Stanton BF, Schor NF, et al, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier; 2011:2061–2065. 3. Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl. 2007;109:8–14. 4. Ashwal S, Russman BS, Blasco PA, et al. Practice parameter: diagnostic assessment of the child with cerebral palsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2004;62:851–863. 5. Rogers L, Wong E. Cerebral palsy. McMaster Pathophysiology Review. 1st ed. 2013. Web site. http://www.pathophys.org/cerebralpalsy/. Accessed May 21, 2014. 6. Levine MS. Cerebral palsy diagnosis in children over age 1 year: standard criteria. Arch Phys Med Rehabil. 1980;61:385–389.
Copyright Ó 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
