Brain injury · 2009
Persistent dysarthria after cefazolin-induced status epilepticus.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lee Yuna, Pyun Sung-Bom, Park Eun Kyung, Youn Sung Won
Аннотация
BACKGROUND: Cefazolin is a well-known antibiotic associated with seizures. However, intrathecal cefazolin-induced status epilepticus (SE) is very rare and resultant persistent dysarthria has not been previously reported.
CASE REPORT: A 66-year-old woman underwent epidural adhesiolysis due to lumbar spinal stenosis and 500 mg of cefazolin was infused through the thecal puncture site during the procedure. SE developed abruptly 40 minutes later and it persisted for 3 days. Severe dysarthria, dysphagia and cognitive dysfunction developed after the cessation of SE. Although the patient's other symptoms showed much improvement after rehabilitation, the dysarthria did not improve after intense speech therapy for 8 months. The brain MRI showed no abnormal findings, but the 2-[(18)F]fluoro-2-deoxy-D-glucose positron emission tomography ((18)F-FDG PET) of the brain demonstrated hypometabolic areas in the bilateral inferior frontal gyrus and the primary motor cortex, representing the oromotor area.
CONCLUSION: Although the exact mechanism underlying the dysarthria is unknown, the dysfunction of the inferior frontal network for speech production revealed by the brain FDG-PET, including the motor speech area (Broca's area), left insula and bilateral primary and premotor cortex representing the oromotor area, might have been responsible for the persistent dysarthria in this patient.
CASE REPORT: A 66-year-old woman underwent epidural adhesiolysis due to lumbar spinal stenosis and 500 mg of cefazolin was infused through the thecal puncture site during the procedure. SE developed abruptly 40 minutes later and it persisted for 3 days. Severe dysarthria, dysphagia and cognitive dysfunction developed after the cessation of SE. Although the patient's other symptoms showed much improvement after rehabilitation, the dysarthria did not improve after intense speech therapy for 8 months. The brain MRI showed no abnormal findings, but the 2-[(18)F]fluoro-2-deoxy-D-glucose positron emission tomography ((18)F-FDG PET) of the brain demonstrated hypometabolic areas in the bilateral inferior frontal gyrus and the primary motor cortex, representing the oromotor area.
CONCLUSION: Although the exact mechanism underlying the dysarthria is unknown, the dysfunction of the inferior frontal network for speech production revealed by the brain FDG-PET, including the motor speech area (Broca's area), left insula and bilateral primary and premotor cortex representing the oromotor area, might have been responsible for the persistent dysarthria in this patient.