CT-guided computer-assisted stereotactic resection of brain tumours

Summary A computer-assisted technique was developed for CT-guided stereotactic microsurgical resection of small intracerebral lesions. An original stereotactic retractor was developed to work with the Riechert-Mundinger's equipment for precise localisation, safe exposure and microsurgical removal of these tumours. A software-program was developed to work on an ordinary IBM-compatible PC/AT. It assisted the procedure from treatment planning till the end, including tumour excision, and provided computerized support for the removal of pathological tissues within the CT-defined boundaries of the lesion.6 patients, harbouring supratentorial intracerebral lesions underwent surgery using this technique. 2 of them suffered from brain metastases, in 1 patient a cavernous angioma was removed, 2 patients had glial tumours, and in the last patient only radiation necrotic tissue was found to be the cause of ring-enhanced lesion, which had been suspected to be a recurrent glioma. Their largest dimensions varied between 18 and 30 mm and the age of the patients ranged from 15 to 52 years. In 2 cases the lesions were localised deeply in the region of basal ganglia and thalamus. In the remaining patients the tumours were rather superficial, infiltrating subcortical white-matter close to the central sulci. There was no mortality nor significant morbidity following the procedure, the Karnofsky Performance Status (KPS) cumulative scores being either unchanged (in 3), or improved (in 3 patients).Current state and modern concepts in image-guided open stereotactic methodology is discussed.     

The prognostic relevance of molecular alterations in glioblastomas for patients age < 50 years

BACKGROUND: In patients with glioblastoma, age < 50 years was identified as a consistent prognostic variable. In addition, the prognosis for these patients may be determined by a complex interaction between age and genetic alterations. The objective of the current study was the molecular analysis of glioblastomas from adult patients age < 50 years ("young adults"). METHODS: The authors analyzed a set of 189 glioblastoma specimens. Fluorescence in situ hybridization was performed with a set of 10 chromosome probes (1p36, 1q25, centomere probe 7 [CEP7], 7p12/epidermal growth factor receptor gene (EGFR), CEP9, 9p21/p16, CEP10, 10q23/phosphatase and tesnin homolog gene (PTEN), 19p13, and 19q13). RESULTS: Patient age < 40 years was associated strongly with a favorable prognosis. Patients age > or = 40 years frequently showed EGFR amplification, loss of 9p, loss of 10q, and gain of chromosome 19. The patients with - 19q were age < 40 years. The survival was shorter for patients with EGFR amplification, gain of chromosome 7, loss of 9p, loss of 10q, and gain of chromosome 19. In contrast, the patients who had tumors with gain of chromosome 9 or loss of 19q had more favorable outcomes. In a multivariate analysis, gain of chromosome 9 (P = 0.026) and loss of 10q23 (P = 0.007) reached the level of independent prognostic value. In addition, the prognostic value of molecular alterations in patients age < 40 years and patients age > 40 years were examined separately. Consequently, EGFR amplification, - 9p, and + 9 were significant for both age groups, whereas gain of chromosome 7 and loss of 10q showed clinical importance only among patients age > 40 years. CONCLUSIONS: Adult patients age < 50 years with glioblastoma had molecularly distinct disease, and the age-dependent heterogeneity seen on the chromosomal level also applied at the clinical level.     

Aspergillosis of the central nervous system (clinical observation and review of literature)

Aspergillosis of the central nervous system presents a challenge faced with the problems arising from the establishing the diagnosis, the low efficiency of treatment, and high mortality rates (about 95% as shown by some data). This paper presents a clinical case of a patient with aspergillosis-induced central nervous system lesion verified by autopsy. Possible errors in the diagnosis and treatment of the patient are analyzed. The literature data including clinical cases, etiopathogenesis, and clinical manifestations and its possible complications are presented. Groups of patients at risk for invasive aspergillosis are considered. The paper gives the data available in the foreign literature on the methods and efficiency of treatment and mortality rates in different groups of patients. The urgency of the problem in the diagnosis and treatment of cerebral aspergillosis rises with the increased number of patients with immunological disorders due to infectious diseases (HIV), social (drug addiction, alcoholism), environmental, and other factors.     

Electrical stimulation of the dorsal periaqueductal gray decreases volume of the brain infarction independently of accompanying hypertension and cerebrovasodilation

We investigated whether selective stimulation of neurons of the sympathoinhibitory ventral periaqueductal gray (VPAG), or sympathoexcitatory dorsal periaqueductal gray (DPAG), differentially modulates CBF and EEG and exerts neuroprotection. Electrical stimulation of either regions of PAG comparably elevated AP and CBF, whereas chemical stimulation with the D,L-homocysteine produced either sympathoinhibition accompanied by decrease in CBF from ventral region or sympathoexcitation accompanied by increase in CBF from dorsal region in nonspinalized rats. The CBF effects evoked from DPAG and VPAG by chemical stimulation were preserved in spinalized rats supporting that the evoked CBF responses result directly from stimulation and are not secondary to AP changes. Stimulation of either region, whether chemical or electrical, synchronized the EEG. To explore whether PAG stimulation might protect the brain against ischemic injury, in other rats the VPAG or DPAG were stimulated for 1 h (50 Hz, 1 s on/1 s off, 75-100 microA) and the middle cerebral artery occluded 72 h later. Stimulation of the DPAG, but not VPAG, significantly reduced infarction volumes relative to sham-stimulated controls as determined 24 h after occlusion. Elevations of AP and CBF did not differ between groups. We conclude: (a). intrinsic neurons of D- and VPAG differentially regulate CBF; (b). neurons of DPAG are neuroprotective independently of changes in CBF and/or AP. The DPAG effect on infarct volume may be related to the central neuroprotective pathway evoked by stimulation of the cerebellar FN.