[Morphology of neurological complications of intravascular lymphomatosis]. / Morphologie neurologischer Komplikationen bei der intravaskulären Lymphomatose.

Intravascular lymphomatosis (IVL) is a rare lymphoproliferative disease characterized by intravascular growth of lymphoma cells in small vessels. Most frequently, its first manifestations occur in the central nervous system or skin. Based on autoptical findings in a 68-year-old-man with IVL, the pathological morphology in the central nervous system is compared to the course of neurological symptoms. The disease could not be diagnosed during his lifetime. The spectrum of neurological deficits can be explained histopathologically by occlusive intravascular aggregations of lymphomatous cells in small vessels of the spinal leptomeninges and nerve roots causing perfusion deficits and areas of ischemic necrosis of up to 4 mm in diameter in the medulla. Aggregations of lymphoma cells in the vessels of other organs are also found, but did not result in clinical symptoms. In reference to the present case, a survey of other literature reports on IVL with neurological and psychiatric manifestations is given. In patients with this condition, even an invasive biopsy has to be considered in order to make the correct diagnosis at an early clinical stage.

The soluble 60-kDa tumour necrosis factor receptor: no difference found between patients with relapsing-remitting multiple sclerosis and controls: increasing levels are associated with the recovery from Guillain-Barré syndrome.

We determined serum and cerebrospinal fluid (CSF) levels of the soluble 60-kDa tumour necrosis factor (TNF) receptor (sTNF-R p60) in 50 patients with relapsing-remitting multiple sclerosis (MS) and in 18 patients with Guillain-Barré syndrome (GBS). Neither in serum nor in CSF samples was there a statistically significant difference between mean receptor concentrations of patients with MS (serum: 1064, SD 262 pg/ml; CSF: 555, SD 130 pg/ml), with other noninflammatory neurological diseases (serum: 1008, SD 248 pg/ml; CSF: 530, SD 112 pg/ml) and with healthy control subjects (serum: 918, SD 180 pg/ml). In order to determine disease activity, magnetic resonance imaging (MRI) of the brain was performed in all MS patients. The mean sTNF-R p60 levels of patients who showed gadolinium DTPA enhancement on MRI were not different from those without enhancement (1034, SD 274 pg/ml vs 1099, SD 248 pg/ml in serum samples and 546, SD 109 pg/ml vs 565, SD 152 pg/ml in CSF samples). In GBS, the sTNF-R p60 levels of serum and CSF samples were significantly higher than in MS and all control groups except for the group with viral meningitis (VM) (GBS: 1544, SD 834 pg/ml in serum, 882, SD 147 pg/ml in CSF; VM: 1518, SD 375 pg/ml in serum, 1131, SD 611 pg/ml in CSF; P < 0.001 for serum samples and P < 0.005 for CSF samples). Serial serum sTNF-R p60 measurements in 13 patients with GBS showed an increase in receptor levels parallel with the recovery from the disease (1276, SD 374 pg/ml at the time of disease onset, 1554, SD 482 pg/ml 14-24 days later and 1787, SD 525 pg/ml after 28-32 days). From our results and the conflicting data of previous studies, we could not agree with the suggestion that the assessment of sTNF-R p60 in MS patients is a useful marker for disease activity. In GBS, subsequently increasing sTNF-R p60 levels are associated with recovery from the disease. It remains to be shown whether they might represent a relevant pathogenetic factor during this stage of GBS.