Determinants of Hip and Femoral Deformities in Children With Spastic Cerebral Palsy

OBJECTIVE: To find factors affecting hip and femoral deformities in children with spastic cerebral palsy (CP) by comparing various clinical findings with imaging studies including plain radiography and computed tomography (CT) imaging. METHODS: Medical records of 709 children with spastic CP who underwent thorough baseline physical examination and functional assessment between 2 to 6 years old were retrospectively reviewed. Fifty-seven children (31 boys and 26 girls) who had both plain radiography of the hip and three-dimensional CT of the lower extremities at least 5 years after baseline examination were included in this study. RESULTS: The mean age at physical examination was 3.6 years (SD=1.6; range, 2–5.2 years) and the duration of follow-up imaging after baseline examination was 68.4 months (SD=22.0; range, 60–124 months). The migration percentage correlated with motor impairment and the severity of hip adductor spasticity (R1 angle of hip abduction with knee flexion). The femoral neck and shaft angle correlated with the ambulation ability and severity of hip adductor spasticity (R1 and R2 angles of hip abduction with both knee flexion and extension). CONCLUSION: Hip subluxation and coxa valga deformity correlated with both dynamic spasticity and shortening of hip adductor muscles. However, we found no correlation between femoral deformities such as femoral anteversion, coxa valga, and hip subluxation.

Correction: Immediate Effect of a Single Session of Whole Body Vibration on Spasticity in Children With Cerebral Palsy

The authors noticed that the original version of the paper contains typographical errors in Figs. 2 and 3.

Immediate Effect of a Single Session of Whole Body Vibration on Spasticity in Children With Cerebral Palsy

OBJECTIVE: To investigate the immediate effect of a single session of whole body vibration (WBV) on lower extremity spasticity in children with cerebral palsy (CP). METHODS: Seventeen children with spastic CP were included. A single session of WBV was administered: 10-minute WBV, 1-minute rest, and 10-minute WBV. The effects of WBV were clinically assessed with the Modified Ashworth Scale (MAS) and Modified Tardieu Scale (MTS) before and immediately, 30 minutes, 1 hour, 2 hours, 3 hours, and 4 hours after WBV. RESULTS: Spasticity of the ankle plantarflexor, as assessed by MAS and MTS scores, was reduced after WBV. Post-hoc analysis demonstrated that, compared to baseline, the MAS significantly improved for a period of 1 hour after WBV, and the R1 and R2–R1 of the MTS significantly improved for a period of 2 hours after WBV. CONCLUSION: A single session of WBV improves spasticity of ankle plantarflexors for 1–2 hours in children with CP. Future studies are needed to test whether WBV is an effective preparation before physiotherapy and occupational therapy.

Cerebral Palsy due to Intracranial Hemorrhage Caused by Consumptive Coagulopathy in Protein C Deficiency: A Case Report / 대한소아신경학회지

Protein C (PROC) is a potent anticoagulant inactivating coagulation factors Va and VIIIa. PROC deficiency is very rare condition inherited as an autosomal dominant or recessive trait, and associated with various thromboembolic and ischemic conditions. Moreover, severe form of PROC deficiency can cause fatal hemorrhagic complications due to consumptive coagulopathy. We reported two children with hemorrhagic stroke who were diagnosed as severe PROC deficiency caused by two different types of compound heterozygous PROC gene mutations. We described results of laboratory tests, genetic analysis, brain magnetic resonance images, and functional outcomes. Both children received prophylactic anticoagulation therapy and presented with purple-colored skin lesions during rehabilitation. Purpura fulminans caused by insufficient anticoagulation should be differentiated from hematoma caused by excessive anticoagulation therapy in these children.

Cerebral Palsy due to Intracranial Hemorrhage Caused by Consumptive Coagulopathy in Protein C Deficiency: A Case Report / 대한소아신경학회지

Protein C (PROC) is a potent anticoagulant inactivating coagulation factors Va and VIIIa. PROC deficiency is very rare condition inherited as an autosomal dominant or recessive trait, and associated with various thromboembolic and ischemic conditions. Moreover, severe form of PROC deficiency can cause fatal hemorrhagic complications due to consumptive coagulopathy. We reported two children with hemorrhagic stroke who were diagnosed as severe PROC deficiency caused by two different types of compound heterozygous PROC gene mutations. We described results of laboratory tests, genetic analysis, brain magnetic resonance images, and functional outcomes. Both children received prophylactic anticoagulation therapy and presented with purple-colored skin lesions during rehabilitation. Purpura fulminans caused by insufficient anticoagulation should be differentiated from hematoma caused by excessive anticoagulation therapy in these children.