ABSTRACT
Hyperacute treatment after onset of cerebral infarction includes tissue plasminogen activator (t-PA）therapy for thrombolysis and endovascular treatment (EVT）with thrombectomy devices. Although reported infrequently, it has been noted that delayed white matter lesions may appear even when recanalization is obtained for occluded blood vessels. We report the rehabilitation progress of a patient treated with t-PA therapy and EVT for right internal carotid artery (ICA）occlusion in whom a delayed white matter lesion appeared in the subacute phase. In this case, EVT was performed after cerebral infarction, and the occluded blood vessel was completely reopened. After hyperacute treatment, mild motor paralysis was observed and basic movements were all assisted, but physical functions and movement abilities improved with continued treatment and rehabilitation. However, consciousness disorder and higher brain dysfunction appeared in the subacute phase, and motor paralysis progressed. This change in symptoms were thought to be due to a delayed white matter lesion that appeared after EVT for cerebral infarction. Physical functions were aggravated, but symptoms improved biphasically. There remain many unclear points about delayed white matter lesions, and there are various reports as to whether or not worsening symptoms eventually improve. Even if imaging shows that a delayed white matter lesion persists, as in this case, symptoms may again recover. Therefore it is necessary to be careful with rehabilitation.
ABSTRACT
Hyperacute treatment after onset of cerebral infarction includes tissue plasminogen activator (t-PA) therapy for thrombolysis and endovascular treatment (EVT) with thrombectomy devices. Although reported infrequently, it has been noted that delayed white matter lesions may appear even when recanalization is obtained for occluded blood vessels. We report the rehabilitation progress of a patient treated with t-PA therapy and EVT for right internal carotid artery (ICA) occlusion in whom a delayed white matter lesion appeared in the subacute phase. In this case, EVT was performed after cerebral infarction, and the occluded blood vessel was completely reopened. After hyperacute treatment, mild motor paralysis was observed and basic movements were all assisted, but physical functions and movement abilities improved with continued treatment and rehabilitation. However, consciousness disorder and higher brain dysfunction appeared in the subacute phase, and motor paralysis progressed. This change in symptoms were thought to be due to a delayed white matter lesion that appeared after EVT for cerebral infarction. Physical functions were aggravated, but symptoms improved biphasically. There remain many unclear points about delayed white matter lesions, and there are various reports as to whether or not worsening symptoms eventually improve. Even if imaging shows that a delayed white matter lesion persists, as in this case, symptoms may again recover. Therefore it is necessary to be careful with rehabilitation.