Slowly progressive dystonia following central pontine and extrapontine myelinolysis.

A 28-year-old woman was hospitalized with dysarthria and oro-mandibular and upper limb dystonia. Approximately 8 years prior to the current admission, the woman became severely hyponatremic due to traumatic subarachnoid hemorrhage-related SIADH. Brain MRIs showed a signal increase in the central pons, thalamus and striatum on T2 weighted images compatible with central pontine and extrapontine myelinolysis. From a few months after that event, dystonia progressed slowly over the subsequent 8 years. We speculate that the particular damage chiefly to the myelin structures by myelinolytic process may have caused an extremely slow plastic reorganization of the neural structures, giving rise to progressive dystonia.

[Acute bacterial meningitis and foramen magnum syndrome as a presentation of odontoid osteomyelitis. A case report].

A 77-year-old male was hospitalized with a 6-day history of severe posterior cervical pain and headache. An initial lumbar puncture revealed polymorphonuclear pleocytosis indicating pyogenic meningitis. The blood and throat cultures on admission were positive for Staphylococcus aureus. A combination of ceftriaxone and ABPC, both of which were sensitive to the pathogen, were intravenously administered for one month, by which he responded well as to the meningitis. However, he was found to have persistent neck pain, and wasting and weakness of the shoulder girdles, which were associated with polyneuropathy-like sensory loss. Neuroimaging studies disclosed a partial destruction of the odontoid process, subluxation of the atlantoaxial joint, MRI evidence of an inflammatory pseudomass formation dorsal to the odontoid process and an increased uptake of radionuclide on bone scanning, all of which were indicative of osteomyelitic processes at the region of the axis; i.e., the meningitis was thought to be secondary to osteomyelitis of the odontoid process and hence the foramen magnum syndrome characteristic to this particular case was explained by the compression of the cervicomedullary junction due to the pseudomass. To our knowledge, this is the first case of primary odontoid osteomyelitis to be reported in Japan.