Two exceptional phenomena in an anaplastic oligo-astrocytoma.
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Biomedical subjects
Publications and source records attributed to W Taal.
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A 78-year-old man with metastasised prostate carcinoma presented with a painless paraparesis. His cerebrospinal fluid showed elevated protein and a mononuclear pleiocytosis, but cytology investigations of 5 separate samples revealed no malignant cells in the cerebrospinal fluid. Extensive viral and bacterial tests (including ELISA for Borrelia burgdorferi) of serum and cerebrospinal fluid were negative. On the day radiation therapy for presumed leptomeningeal metastases was due to start the IgG and IgM Western blot for Borrelia were found to be positive, indicating neuroborreliosis. Soon after the start of antibiotic therapy the paraparesis began to improve and after four weeks the patient had made a complete recovery. In patients with a progressive paraparesis, neuroborreliosis should be considered even in the absence of pain.
A 27-year-old woman with a history of aplastic anaemia complained of poor control of her right arm and hand, unsteady gait, and headache that increased while in a recumbent position. She was diagnosed with cerebral sinus thrombosis. Additional investigation revealed paroxysmal nocturnal haemoglobinuria (PNH). Treatment with heparin was initiated but stopped after the patient developed a brain haemorrhage. The patient recovered with no signs of residual symptoms and began taking oral anticoagulants as maintenance therapy. PNH is a rare acquired clonal disorder due to a defective expression of the glycosylphosphatidyl-inositol anchor membrane protein. It is characterised by haemolytic anaemia, diminished haematopoiesis, increased susceptibility for infections and a hypercoagulable state. Patients with aplastic anaemia have an increased risk of developing PNH. In patients with cerebral sinus thrombosis PNH should be considered as a possible underlying disorder. These patients should be questioned for possible clinical symptoms of PNH, such as acute abdominal pain or dark urine in the morning. For patients with these symptoms and in those with a history of aplastic anaemia or recurrent thrombosis, additional testing for PNH should be conducted.
OBJECTIVE: To describe the results of the treatment of recurrent glioma with temozolomide. DESIGN: Retrospective. METHOD: This study evaluated 77 patients with a recurrent high-grade glioma who from August 1997-December 2003 were treated with temozolomide (150-200 mg/m2/day for 5 days per 28-day cycle) following surgery and radiotherapy at the Daniel den Hoed Oncology Centre of the Erasmus MC, Rotterdam, the Netherlands. The patients were divided into 4 groups depending on histology and chemotherapy history. RESULTS: 15 patients received temozolomide for a recurrent anaplastic oligodendroglioma or mixed oligo-astrocytoma. The response in this group was 80% and after 12 months in 47% of the patients there was no disease progression. 35 patients underwent second-line chemotherapy with temozolomide after earlier chemotherapy with procarbazine, lomustine and vincristine for recurrent anaplastic oligodendroglioma or mixed oligo-astrocytoma. Response was 26% and after 12 months in 15% of patients there was still no disease progression. 14 patients were treated with temozolomide for a recurrent anaplastic astrocytoma with a response of 35% and after 12 months in 8% of these patients there was no disease progression. Of the 13 patients with a recurrent glioblastoma who were treated with temozolomide 16% responded and after 6 and 12 months 21% were still free from progression. Temozolomide was well-tolerated: 2 patients had to stop because of probable side effects. CONCLUSION. Temozolomide has an acceptable safety profile and may be regarded as the preferred treatment for recurrent anaplastic gliomas after radiotherapy. There is only a limited role for temozolomide in the treatment of recurrent glioblastoma.
A 23-year-old woman with mild psychomotor retardation presented with fever, coughing, reduced consciousness and a stiff neck. A chest X-ray revealed an infiltrate in the left lower lobe; the cerebrospinal fluid was cloudy with a mild pleocytosis. Ceftriaxone was prescribed and the fever subsided. On the second day of admission she had a seizure, and a paraparesis emerged. Despite changes in the antibiotic regimen, her clinical condition hardly improved. On the fifth day, antibodies against Mycoplasma pneumoniae were found to be strongly positive and the diagnosis was M. pneumoniae infection. This accounted for the pneumonia together with meningoencephalitis and a transverse myelitis. The antibiotics were switched to doxycycline and the clinical condition improved dramatically. Six weeks after discharge, the patient had made a complete recovery. In patients suffering from meningitis with an atypical presentation, uncommon causes of infection should be considered. Together with a pneumonia, M. pneumoniae, Chlamydia pneumoniae, Legionella pneumophila and Listeria monocytogenes should be high on the list of potential causes for bacterial meningitis.
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In this ultrastructural study the colocalization of gamma-amino butyric acid (GABA) and glycine in terminals within cat lumbar motoneuronal cell groups was investigated and the frequency of this colocalization was determined. For this purpose the post-embedding immunogold technique was applied on serial sections, using antibodies directed against either GABA or glycine. Analysis of all labelled terminals in a random area of cat motoneuronal cell groups showed that 25 +/- 5% were labelled for GABA only, 29 +/- 6% were labelled for glycine only and 46 +/- 9% were labelled for both GABA and glycine, meaning that nearly two out of every three GABA-labelled terminals were also labelled for glycine and vice versa. Based on these results and on other data suggesting a high frequency of colocalization, it is concluded that in cat motoneuronal cell groups colocalization of GABA and glycine is the rule rather than the exception.