No to shinkei = Brain and nerve最新文献

Taking into account how to care patients at home with intractable neurological disease and their family, I have introduced the achievement of the medical caring technique by an aged family member, the risks of the PEG and acute respiratory failures under BiPAP, the problems in home rehabilitation, and the experiences of home terminal care, from the view point of a practicing physician. Home caring pursues to support patients and their family to live peacefully with disease with highest quality of life. Hospice caring is also an important issue. From now on, I would like to try to give even better home care by early recognition of problems and by cooperating with hospitals, clinics and other field workers.

Complex regional pain syndrome type I (CRPS-I) requires the presence of regional pain and sensory changes associated with findings such as abnormal skin color, temperature change, sudomotor activity, or edema, following a noxious event. Complex regional pain syndrome type I induced by phenobarbital (PB) is not well known, although several reports have strengthened the association between PB and CRPS-I. I reviewed the charts of 99 patients treated with PB to assess the incidence, clinical characteristics, investigations, dosage and plasma concentration of PB, and risk factors in the development of CRPS-I. Six patients developed CRPS-I. Pain was severe and allodynia, swelling, discoloration, sweating were present in all patients. This syndrome manifested bilaterally in some patients. Affected patients included 5 men and 1 woman between the ages of 52 and 78 (average 64.2 years). A radiograph showed demineralization in one patient. Thermography showed temperature differences between affected and unaffected limbs, although in a few patients the differences were little because of bilateral affected limbs. 99Technetium methlyene diphosphonate bone scan showed increased periarticular changes in most of the patients. The patients developed CRPS-I at 9.7 weeks (average) after PB was begun. The average time was 7.5 months between CPRS-I and PB reduction. Neither sympathetic ganglion blockade nor physical therapy was effective. Treatment of CRPS-I consists of PB reduction and prednisone and/or Neurotropin. In all patients clinical symptoms and signs such as pain and edema, and range of motion of their shoulders were improved after PB discontinuation. One patient was followed longitudinally, documenting improvement following discontinuation, reexacerbation with PB rechallenge, and remission once more when PB were discontinued. The higher incidence should depend on the coexistence of separate risk factors such as age and PB dosage. Recognition of CRPS-I induced PB, early diagnosis, and withdrawal of PB are important for symptomatic relief and improvement of QOL.

We report two cases of myelitis associated with Sjögren syndrome without xerosis. Case 1: A 30-year old woman developed dysesthesia on both upper extremities and weakness of the right arm. A T2-weighted MRI examination showed a high-intensity signal and a swollen lesion between the first and seventh cervical vertebral levels. She was diagnosed as having primary Sjögren syndrome based on the positive finding of a Saxon test, typical salivary gland scintigraphy findings, and an elevated anti-SS-A antibody titer. We suspected that her myelitis was associated with Sjögren syndrome and treated her using steroid therapy. Although her symptoms were alleviated, her myelitis relapsed at the same location after the cessation of steroid therapy. Case 2: A 31-year-old woman developed dysesthesia on her neck and both upper extremities and exhibited tonic spasm. A T2-weighted MRI examination showed a high-intensity signal and a swollen lesion between the first and sixth cervical vertebral levels. She was diagnosed as having primary Sjögren syndrome based on the positive findings of a Rose Bengal test, a Schirmer's test, and a Saxon test as well as typical salivary gland scintigraphy findings and elevated titers of anti-SS-A and anti-SS-B antibodies. We suspected that her myelitis was associated with Sjögren syndrome and treated her using steroid therapy. Her symptoms improved after steroid therapy. Based on these two cases, we concluded that MRI findings for myelitis associated with Sjögren syndrome are characterized by a swollen lesion of more than three vertebral segments in length, and the relapse tends to occur at the same location.

We report a fatal case of meningoencephalitis due to Listeria monocytogenes. A 74-year old alcoholic man presented with high-grade fever lasting for four days without headache and meningeal signs. Routine blood analysis showed leukocytosis, but serum C-reactive protein (CRP) was not significantly elevated. He developed altered consciousness with focal seizure, and cerebrospinal fluid (CSF) examination showed a minor degree of pleocytosis, elevated protein, and hypoglycorrhachia. Repeated CSF examination four days later showed greater increases in cells and proteins as well as severely decreased glucose level. Bacterial culture from the initial CSF showed a growth of L. monocytogenes. Meningoencephalitis caused by L. monocytogenes may have atypical clinical and laboratory features, and should be listed in the differential diagnosis of immunocompromised or elderly patients presenting with fever of unknown origin associated with altered consciousness.

We reported a 60-year-old woman who suffered from isolated neurosarcodosis. She was presenting comprehensive dysfunction and intermittent high fever. In several months she gradually developed dysorientation, amnesia, dementia. However, no focal sign such as paralysis or sensory disturbance was demonstrated. Her blood chemistry showed normal including ACE (angiotensin converting enzyme) and lysozyme. Cerebrospinal fluid revealed elevated mononuclear cells, protein, and decreased glucose level. At first we treated with antibiotics including antiviral drugs in suspect of the infectious encephalomeningitis. But no improvement was observed. The elevation of ACE in spinal fluid made us suspect of neurosarcoidosis. So intravenous predonizoron (1,000 mg) was given, improving. Her high fever and mental disturbance improved. Second spinal fluid showed improvement. During the course her brain MRI revealed new bilateral diffuse confluent high intensity lesions at the deep white matters. Brain biopsy of deep matter at the right anterior lobe showed noncaseating granuloma. Since systemic work-up to detect sarcoidosis did not reveal lesions other than CNS, we considered this patient as having isolated CNS sarcoidosis.