ABSTRACT
Our objective is to evaluate the applicability of segmental phase angle (PhA) via bioelectrical impedance analysis (BIA) for post-stroke complex regional pain syndrome (CRPS). Due to its noninvasiveness and convenience, various studies have used BIA in clinical conditions. We measured segmental PhA in 4 patients at the time of CRPS diagnosis and repeated 4 weeks after 2 weeks of steroid pulse therapy. In 3 cases, the affected-to-unaffected ratio of the upper limb PhA decreased at the time of diagnosis. In 2 cases with improvement of more than 5 points in the CRPS severity score (CSS), increased ratios were observed. In other 2 cases with improvement of less than 4 points in the CSS, no remarkable changes in the ratios were found. We suggest that the segmental PhA can be helpful in assessment of post-stroke CRPS and its recovery.
ABSTRACT
Our objective is to evaluate the applicability of segmental phase angle (PhA) via bioelectrical impedance analysis (BIA) for post-stroke complex regional pain syndrome (CRPS). Due to its noninvasiveness and convenience, various studies have used BIA in clinical conditions. We measured segmental PhA in 4 patients at the time of CRPS diagnosis and repeated 4 weeks after 2 weeks of steroid pulse therapy. In 3 cases, the affected-to-unaffected ratio of the upper limb PhA decreased at the time of diagnosis. In 2 cases with improvement of more than 5 points in the CRPS severity score (CSS), increased ratios were observed. In other 2 cases with improvement of less than 4 points in the CSS, no remarkable changes in the ratios were found. We suggest that the segmental PhA can be helpful in assessment of post-stroke CRPS and its recovery.
ABSTRACT
Pantothenate kinase-associated neurodegeneration (PKAN) is a neurodegenerative disorder characterized by iron accumulation in the globus pallidus (GP) of the brain (neurodegeneration with brain iron accumulation [NBIA]), which is characterized by dystonia and spasticity resulting in postural difficulties. A 33-month-old boy was admitted with a pronounced gait disturbance. Marked hypertonicity in the patient's both calf muscles was noted, resulting in waddling with repeated slip-falls. NBIA was suspected by high T2 intensity in the GP on brain MRI, then it was confirmed by detecting PANK2 mutation. Botulinum toxin-A injection was administered to both calf muscles. After 2 weeks, a decrease in spasticity and an increase in range of motion were observed, and consequently, an increase in the patient's gait stability with both heels touching the ground, enabling him to walk straight independently. A definitive treatment for NBIA has not been established, and a symptomatic therapy is currently the mainstay of treatment in this case. This is the first case report of botulinum toxin injection for treatment of gait disturbance caused by spasticity in an infantile-onset PKAN.