Introduction. Serological confirmation of an infectious acute myelitis injury is difficult to confirm as it is sometimes due to a post-infectious etiology. Objectives. The aim of this study was to define the clinical,...Introduction. Serological confirmation of an infectious acute myelitis injury is difficult to confirm as it is sometimes due to a post-infectious etiology. Objectives. The aim of this study was to define the clinical, biological and pr ognostic patterns of infectious myelitis. Patients and methods. This retrospecti ve study included 153 subjects hospitalized in the department of neurology betwe en 1993 and 2002 for treatment of a noncompressive acute myelopathy. Biological confirmation of recent infection was obtained in 12 patients (8 p. 100). Results . An infectious syndrome, beginning prior to the neurological symptoms, was foun d in 67 percent of patients. The clinical symptoms were severe with loss of sens oromotor and sphincter functions and ascending spinal cord dysfunction (acute tr ansverse myelopathy). Spinal cord MRI showed extended centromedullar high intens ity signals with rapid and complete regression. CSF analysis cell count was abov e 30/mm3 with hyperproteinorachia, in 75 percent and 58 percent of patients resp ectively. CSF electrophoresis did not detect oligoclonal bands. Clinical outcome was good in all patients except one, however sphincter disorders recovered slow ly. Discussion. Our study illustrates a stereotypical clinical, biological and p rognostic pattern for infectious acute myelitis. These findings contribute signi ficantly to therapeutic decision making and establishing prognosis at the initia l phase of acute myelopathy.展开更多
文摘Introduction. Serological confirmation of an infectious acute myelitis injury is difficult to confirm as it is sometimes due to a post-infectious etiology. Objectives. The aim of this study was to define the clinical, biological and pr ognostic patterns of infectious myelitis. Patients and methods. This retrospecti ve study included 153 subjects hospitalized in the department of neurology betwe en 1993 and 2002 for treatment of a noncompressive acute myelopathy. Biological confirmation of recent infection was obtained in 12 patients (8 p. 100). Results . An infectious syndrome, beginning prior to the neurological symptoms, was foun d in 67 percent of patients. The clinical symptoms were severe with loss of sens oromotor and sphincter functions and ascending spinal cord dysfunction (acute tr ansverse myelopathy). Spinal cord MRI showed extended centromedullar high intens ity signals with rapid and complete regression. CSF analysis cell count was abov e 30/mm3 with hyperproteinorachia, in 75 percent and 58 percent of patients resp ectively. CSF electrophoresis did not detect oligoclonal bands. Clinical outcome was good in all patients except one, however sphincter disorders recovered slow ly. Discussion. Our study illustrates a stereotypical clinical, biological and p rognostic pattern for infectious acute myelitis. These findings contribute signi ficantly to therapeutic decision making and establishing prognosis at the initia l phase of acute myelopathy.
