We report on a stroke patient who showed delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage. This 32-year-old female patient underwent craniotomy and drainage for right intracere...We report on a stroke patient who showed delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage. This 32-year-old female patient underwent craniotomy and drainage for right intracerebral hemorrhage due to rupture of an arteriovenous malformation. Brain MR images revealed a large leukomalactic lesion in the right fronto-parietal cortex. Diffusion tensor tractography at 8 months after onset revealed that the right corticospinal tract was severely injured. At this time, the patient could not stand or walk despite undergoing rehabilitation from 2 months after onset. It was believed that severe spasticity of the left leg and right ankle was largely responsible, and thus, antispastic drugs, antispastic procedures （alcohol neurolysis of the motor branch of the tibial nerve and an intramuscular alcohol wash of both tibialis posterior muscles） and physical therapy were tried to control the spasticity. These measures relieved the severe spasticity, with the result that the patient was able to stand at 3 months. In addition, the improvements in sensorimotor function, visuospatial function, and cognition also seemed to contribute to gait recovery. As a result, she gained the ability to walk independently on even floor with a left ankle foot orthosis at 11 months after onset. This case illustrates that clinicians should attempt to find the cause of gait inability and to initiate intensive rehabilitation in stroke patients who cannot walk at 3-6 months after onset.展开更多
基金supported by the 2012 Yeungnam University Research Grant
文摘We report on a stroke patient who showed delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage. This 32-year-old female patient underwent craniotomy and drainage for right intracerebral hemorrhage due to rupture of an arteriovenous malformation. Brain MR images revealed a large leukomalactic lesion in the right fronto-parietal cortex. Diffusion tensor tractography at 8 months after onset revealed that the right corticospinal tract was severely injured. At this time, the patient could not stand or walk despite undergoing rehabilitation from 2 months after onset. It was believed that severe spasticity of the left leg and right ankle was largely responsible, and thus, antispastic drugs, antispastic procedures （alcohol neurolysis of the motor branch of the tibial nerve and an intramuscular alcohol wash of both tibialis posterior muscles） and physical therapy were tried to control the spasticity. These measures relieved the severe spasticity, with the result that the patient was able to stand at 3 months. In addition, the improvements in sensorimotor function, visuospatial function, and cognition also seemed to contribute to gait recovery. As a result, she gained the ability to walk independently on even floor with a left ankle foot orthosis at 11 months after onset. This case illustrates that clinicians should attempt to find the cause of gait inability and to initiate intensive rehabilitation in stroke patients who cannot walk at 3-6 months after onset.
