Cerebral palsy physical examination

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:  Iqra Qamar M.D.[2]

## Overview

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Patients with cerebral palsy usually have abnormal neck or truncal tone, asymmetric posture, abnormal strength, gait and coordination. Physical examination of patients with cerebral palsy is usually remarkable for neuromuscular findings such as tremors or involuntary movements, athetosis, chorea, muscle rigidity, sensory loss, diplegia/hemiplegia/quadriplegia, intellectual disability, dystonia, normal/increased/decreased tone, persistent or asymmetric fisting, abnormal oromotor patterns, tongue retraction and thrust, tonic bite, oral hypersensitivity, grimacing, poor head control and spastic cerebral palsy presents with features of upper motor neuron lesion.

## Physical Examination

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CP: Cerebral palsy; PVL: Periventricular leukomalacia; SGA: Small for gestational age.

Type of motor dysfunction  | Common causes  | Percentage of CP cases  | Age at which infants affected  | Clinical findings

|
|
|
|

Spastic

(Pyramidal) subtypes

| Spastic diplegia |

* Most commonly associated with PVL

| 13 to 25%  |

* Preterm infants
* Risk increases with decreasing gestational age

* Lower limbs are more affected than the upper limbs
* Affected patients have flexion, adduction, and internal rotation of the hips with contractures of the hip flexors and hamstring muscles
* Variable degrees of flexion at the elbows and knees
* Reduced limb length and muscle bulk in lower extremities

Spastic hemiplegia |

* Neonatal stroke
* Prenatal circulatory disturbances
* Brain development problems

| 21 to 40%  |

* Term infants of normal birth weight

* One side of the body is affected
* The arm typically is more affected than the leg
* The arm is adducted at the shoulder and flexed at the elbow, the forearm is pronated, and the wrist and fingers are flexed with the hand closed
* The hip is partially flexed and adducted, and the knee and ankle are flexed; the foot may remain in the equinovarus or calcaneovalgus position
* Most children also have sensory deficits
* In mildly affected patients, postural abnormalities are more apparent during walking or running; however, unless severe intellectual disability is present, independent walking usually occurs at the appropriate age or is only slightly delayed

Spastic quadriplegia |

* [[|TORCH|Congenital infection]]
* Cerebral dysgenesis
* Perinatal or postnatal events

| 20 to 43%  |

* Most commonly term SGA infants, but can also occur in preterm infants

* All limbs are affected
* Upper limbs may be equally or more involved than lower limbs
* Children often are severely handicapped
* Feeding difficulties, chronic respiratory insufficiency, and seizure are common

Dyskinetic (extra-pyramidal) subtypes |

* Most cases are caused by severe perinatal asphyxia resulting in injury to the thalamus, basal ganglia, hippocampus, reticular formation, and/or cerebellum
* Severe hyperbilirubinemia (kernicterus) can cause choreoathetotic CP

| 12 to 14%  |

* Predominantly term infants

| Choreoathetotic CP:

* Chorea consists of rapid, irregular, unpredictable contractions of individual muscles or small muscle groups that involve the face, bulbar muscles, proximal extremities, and fingers and toes
* Athetosis consists of slow, smooth, writhing movements that involve distal muscles
* Movements may be induced or accentuated by emotion or change in posture
* Athetosis is most apparent during reaching
* Stress, excitement, or fever may exacerbate chorea
* Primitive reflexes often are retained
* Oropharyngeal difficulties occur commonly

Dystonic CP:

* Repetitive, patterned, twisting, and sustained movements of the trunk and limbs that may be either slow or rapid
* Pyramidal signs and anarthria may occur
* "Tension", a sudden involuntary increase in tone affecting both flexor and extensor muscles, may occur during attempted movement or with emotion
* Tendon reflexes are normal or may be difficult to elicit
* Clonus and extensor plantar responses are absent

Ataxic CP |

* Most cases are caused by early prenatal events
* Etiology is frequently unknown
* Some cases have genetic causes, including:
* Cerebellar hypoplasia
* Granule cell deficiency
* Joubert syndrome
* Rarely associated with congenital hypoplasia of the cerebellum

| 4 to 13%  |

* Term infants

* Ataxic movements
* Widespread disorder of motor function
* Ataxia usually improves with time
* Speech typically is slow, jerky, and explosive

#### Developmental milestones:

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* The most common delayed motor milestones are:
* Unable to sit by 8 months
* Unable to walk by 18 months
* Hand preference at < 1yr age

### Appearance of the Patient

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* General physical examination may show:
* Abnormal neck or truncal tone
* Asymmetric posture
* Abnormal strength
* Abnormal gait
* Abnormal coordination
* Cerebral palsy involves a non-progressive motor dysfunction affecting muscle tone, posture and movement. On physical examination, following findings may be observed:[1][2][3][4][5][6][7][8]
* Serial examinations are required to make a definitive diagnosis as the maturation of nervous system continues even after birth resulting in evolvement of neurological function and functioning ability.

### HEENT

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* Dysarthria
* Abnormal hearing tests
* Visual abnormalities

### Lungs

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* Decreased chest expansion
* Fine/coarse crackles upon auscultation of the lung bases unilaterally/bilaterally
* Rhonchi
* Wheezing may be present

### Heart

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* S1
* S2

### Abdomen

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* Guarding may be present

### Back

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* Scoliosis

### Neuromuscular

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* Tremors or involuntary movements
* Athetosis -slow, writhing movements
* Chorea[9]
* Muscle rigidity
* Sensory loss
* Diplegia/hemiplegia/quadriplegia[10][11]
* Intellectual disability
* Dystonia[12]
* Tone may be normal/increased/decreased
* Persistent or asymmetric fisting
* Abnormal oromotor patterns
* Tongue retraction and thrust
* Tonic bite
* Oral hypersensitivity
* Grimacing
* Poor head control
* Spastic cerebral palsy presents with features of upper motor neuron lesion that includes:[1][13][14]
* Positive signs:
* Muscle spasticity
* Clonus may be present
* Hyperreflexia
* Extensor muscle response
* Negative signs such as:
* Fatigue
* Weakness
* Slow, effortful voluntary movements
* Impaired fine-motor function
* Difficulty in isolating individual movement
* Abnormal gait: Walking on toes/ a crouched gait/ a scissors-like gait with knees crossing/ a wide gait or an asymmetrical gait
* Persistence or exaggeration of primitive reflexes such as:
* Moro reflex (startle reflex)
* Asymmetric tonic neck reflexes (fencing posture with neck turned in same direction when one arm is extended and the other is flexed)
* Other reflexes that might be noticed include:
* Symmetric tonic neck reflex
* Palmar grasp reflex
* Tonic labyrinthine reflex
* Foot placement reflex
* Underdevelopment/disappearance/absence of postural or protective reflexes (extending arm when sitting up)

### Extremities

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* Common findings seen in cerebral palsy on hip, knee and foot joint are as follows:
* Hip
* Excessive flexion
* Adduction
* Femoral anteversion
* Knee
* flexion and extension with valgus or varus stress
* Foot
* Equinus or toe walking
* Varus or valgus of the hindfoot
* Spastic diplegia may involve
* flexion at the elbows and knees
* flexion, adduction, and internal rotation of the hips
* Equinovalgus or calcaneovarus deformity of the foot
* Atrophy below the waist[15]
* Spastic hemiplegia
* Shoulder retraction and flexion of fingers with adduction of the thumb
* Hip is partially flexed and adducted with flexed ankle and knee[16]
* Chorea
* Athetosis
* Ataxia[17]

## References

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1. ↑ 1.0 1.1 Myklebust BM (1990). "A review of myotatic reflexes and the development of motor control and gait in infants and children: a special communication". Phys Ther. 70 (3): 188–203. PMID 2304976.
2. ↑ Rosenbloom L (2007). "Definition and classification of cerebral palsy. Definition, classification, and the clinician". Dev Med Child Neurol Suppl. 109: 43. PMID 17370483.
3. ↑ Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, Damiano D, Dan B, Jacobsson B (2007). "A report: the definition and classification of cerebral palsy April 2006". Dev Med Child Neurol Suppl. 109: 8–14. PMID 17370477.
4. ↑ "Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Surveillance of Cerebral Palsy in Europe (SCPE)". Dev Med Child Neurol. 42 (12): 816–24. 2000. PMID 11132255.
5. ↑ Capute AJ (1979). "Identifying cerebral palsy in infancy through study of primitive-reflex profiles". Pediatr Ann. 8 (10): 589–95. PMID 492783.
6. ↑ Zafeiriou DI, Tsikoulas IG, Kremenopoulos GM (1995). "Prospective follow-up of primitive reflex profiles in high-risk infants: clues to an early diagnosis of cerebral palsy". Pediatr. Neurol. 13 (2): 148–52. PMID 8534280.
7. ↑ Noritz GH, Murphy NA (2013). "Motor delays: early identification and evaluation". Pediatrics. 131 (6): e2016–27. doi:10.1542/peds.2013-1056. PMID 23713113.
8. ↑ Allen MC, Alexander GR (1997). "Using motor milestones as a multistep process to screen preterm infants for cerebral palsy". Dev Med Child Neurol. 39 (1): 12–6. PMID 9003724.
9. ↑ Harbord MG, Kobayashi JS (1991). "Fever producing ballismus in patients with choreoathetosis". J. Child Neurol. 6 (1): 49–52. doi:10.1177/088307389100600111. PMID 2002202.
10. ↑ Himmelmann K, Beckung E, Hagberg G, Uvebrant P (2006). "Gross and fine motor function and accompanying impairments in cerebral palsy". Dev Med Child Neurol. 48 (6): 417–23. doi:10.1017/S0012162206000922. PMID 16700930.
11. ↑ Odding E, Roebroeck ME, Stam HJ (2006). "The epidemiology of cerebral palsy: incidence, impairments and risk factors". Disabil Rehabil. 28 (4): 183–91. doi:10.1080/09638280500158422. PMID 16467053.
12. ↑ Sanger TD, Chen D, Fehlings DL, Hallett M, Lang AE, Mink JW, Singer HS, Alter K, Ben-Pazi H, Butler EE, Chen R, Collins A, Dayanidhi S, Forssberg H, Fowler E, Gilbert DL, Gorman SL, Gormley ME, Jinnah HA, Kornblau B, Krosschell KJ, Lehman RK, MacKinnon C, Malanga CJ, Mesterman R, Michaels MB, Pearson TS, Rose J, Russman BS, Sternad D, Swoboda KJ, Valero-Cuevas F (2010). "Definition and classification of hyperkinetic movements in childhood". Mov. Disord. 25 (11): 1538–49. doi:10.1002/mds.23088. PMC 2929378. PMID 20589866.
13. ↑ Burke D (1988). "Spasticity as an adaptation to pyramidal tract injury". Adv Neurol. 47: 401–23. PMID 3278524.
14. ↑ Landau WM (1988). "Clinical neuromythology II. Parables of palsy pills and PT pedagogy: a spastic dialectic". Neurology. 38 (9): 1496–9. PMID 3412602.
15. ↑ Lesný I, Stehlík A, Tomásek J, Tománková A, Havlícek I (1993). "Sensory disorders in cerebral palsy: two-point discrimination". Dev Med Child Neurol. 35 (5): 402–5. PMID 8495821.
16. ↑ Cooper J, Majnemer A, Rosenblatt B, Birnbaum R (1995). "The determination of sensory deficits in children with hemiplegic cerebral palsy". J. Child Neurol. 10 (4): 300–9. doi:10.1177/088307389501000412. PMID 7594266.
17. ↑ Miller G, Cala LA (1989). "Ataxic cerebral palsy--clinico-radiologic correlations". Neuropediatrics. 20 (2): 84–9. doi:10.1055/s-2008-1071271. PMID 2739880.

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