Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fractures are a serious complication after stroke. Among patients with femoral neck fractures, a large subgroup have had a previous stroke. This study aimed to investigate the incidence of fractures after stroke. Included in the study were 1139 patients consecutively admitted for acute stroke. Fractures occurring from stroke onset until the end of the study or death were registered retrospectively. Hip fracture incidence was compared with corresponding rates from the general population. Patients were followed up for a total of 4132 patient-years (median 2.9 years). There were 154 fractures in 120 patients and median time between the onset of stroke and the first fracture was 24 months. Women had significantly more fractures than men (chi 2 = 15.6; p < 0.001). In patients with paresis most of the fractures affected the paretic side (chi 2 = 22.5; p < 0.001) and 84% of the fractures were caused by falls. Hip fracture was the most frequent fracture and the incidence was 2-4 times higher in stroke patients compared with the reference population. Fractures are thus a common complication after stroke. They are usually caused by falls and affect the paretic side. It is necessary to focus on the prevention of post-stroke fractures, including the prevention of both falls and osteoporosis.
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PMID:Fractures after stroke. 969 83

This study investigated the kinetic strategy and compensatory mechanisms during self-ambulatory gait in children with lumbo-sacral myelomeningocele. Thirty-one children with mid-lumbar to low-sacral myelomeningocele who walked without aids and 21 control children were evaluated by three-dimensional gait analysis. Joint moments in all planes at the hip and knee and sagittal moments at the ankle, as well as joint power and work done at all three joints, were analyzed. Joint moment capacity lost due to plantarflexor and dorsiflexor weakness was provided instead by orthotic support, but other joints were loaded more to compensate for the weakness at the ankles and restricted ankle motion. Subjects with total plantarflexor and dorsiflexor paresis and strength in the hip abductors had more knee extensor loading due to plantarflexor weakness and dorsiflexion angle of the orthotic ankle joint. The subjects with orthoses also generated more power at the hip to supplement the power generation lost to plantarflexor weakness and fixed ankles. The most determinant muscle whose paresis changes gait kinetics was the hip abductor. Hip abductor weakness resulted in a characteristic pattern where the hips displayed an eccentric adduction moment, mediating energy transfer into the lower limbs, and the hips replaced the knees as power absorbers in early stance. Joint moment, power and work analyses complement a kinematic analysis to provide a complete picture of how children who have muscle paresis recruit stronger muscle groups to compensate for weaker ones.
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PMID:Kinetics of compensatory gait in persons with myelomeningocele. 1553 30