Hyeok Gyu Kwon1, Sung Ho Jang. 1. Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University , Namku, Taegu , Republic of Korea.
Abstract
BACKGROUND: Many studies have demonstrated neural injury in patients with mild traumatic brain injury, using diffusion tensor imaging (DTI). However, knowledge regarding injury of the corticoreticular pathway (CRP) is limited. This study reports on a patient with mild TBI who showed delayed gait disturbance due to injury of the CRP following head trauma, which was demonstrated by DTI. METHODS: A 14-year-old female patient suffered from an in-car accident: her head was hit with the backseat during hyperextension after flexion movement when her sedan was struck by another sedan from behind. She showed mild quadriparesis after onset. At 29 days after onset, she noted gait disturbance and aggravated quadriparesis with more severe weakness of the proximal joints. RESULTS: No abnormality was observed on brain MRI and electromyography study performed at 10 weeks after onset. Both CRPs were discontinued at the midbrain level on 10-week DTI. CONCLUSION: It appears that the proximal weakness of this patient was attributed to injury of both CRPs following head trauma. It is assumed that the mild weakness at the onset of head trauma was caused by the primary traumatic axonal injury and the aggravated weakness that started from 29 days might be ascribed to the secondary traumatic axonal injury.
BACKGROUND: Many studies have demonstrated neural injury in patients with mild traumatic brain injury, using diffusion tensor imaging (DTI). However, knowledge regarding injury of the corticoreticular pathway (CRP) is limited. This study reports on a patient with mild TBI who showed delayed gait disturbance due to injury of the CRP following head trauma, which was demonstrated by DTI. METHODS: A 14-year-old female patient suffered from an in-car accident: her head was hit with the backseat during hyperextension after flexion movement when her sedan was struck by another sedan from behind. She showed mild quadriparesis after onset. At 29 days after onset, she noted gait disturbance and aggravated quadriparesis with more severe weakness of the proximal joints. RESULTS: No abnormality was observed on brain MRI and electromyography study performed at 10 weeks after onset. Both CRPs were discontinued at the midbrain level on 10-week DTI. CONCLUSION: It appears that the proximal weakness of this patient was attributed to injury of both CRPs following head trauma. It is assumed that the mild weakness at the onset of head trauma was caused by the primary traumatic axonal injury and the aggravated weakness that started from 29 days might be ascribed to the secondary traumatic axonal injury.