Multifocal epithelioid hemangioendothelioma derived from the spine region: case report and literature review.

BACKGROUND: Epithelioid hemangioendothelioma (EHE) is a rare vascular tumor with malignant biological behavior. It arises from endothelial cells, usually within soft tissues, and can occur in almost all locations. CASE REPORT: We report a unique case of a 25-year-old man who presented with sudden attacks of severe back pain followed by acute non-traumatic paraplegia. Emergency diagnostics revealed a pathologic fracture of the T7 vertebra with tumor tissue invasion of the spinal canal. Furthermore, multifocal metastases were found. RESULTS: To achieve en bloc resection, interdisciplinary surgical approaches were indicated. Despite multimodal therapy concepts, including radiotherapy and chemotherapy as well as endovascular embolization, the patient died within 8 weeks. CONCLUSION: Prognosis of EHE is unpredictable and mainly determined by its location. The lesions are potentially aggressive; therefore, en bloc resection should be attempted whenever possible. However, as shown in the literature, only 15% of patients are suitable for total resection.

Intraoperative MRI for interventional neurosurgical procedures and tumor resection control in children.

INTRODUCTION: Despite the introduction of neuronavigational systems, radical tumor removal is still problematic in many neurosurgical procedures. Thus, direct intraoperative imaging for tumor resection control was implemented with an intraoperative magnetic resonance imaging (ioMRI) scanner installed in the operating room. Whereas most procedures with ioMRI were carried out in adults, we summarize 7 years of experience using ioMRI in children for interventional neurosurgical procedures or for tumor resection control. METHOD: An open magnetic resonance scanner (Magnetom Open 0.2 T) was installed in the neurosurgical operating room. For tumor resection control, ioMRI was performed in 35 procedures. After the ioMRI scans were analyzed with respect to quality, the identification of residual tumor was considered by the attending neuroradiologist and neurosurgeon. If residual tumor tissue was present, a new three-dimensional (3D) dataset was acquired to update the neuronavigation; subsequently, the tumor resection was extended. In all these procedures, the results of the ioMRI were checked by an early postoperative high-field magnetic resonance imaging (MRI) study. In addition, ioMRI was carried out in ten other children to monitor interventional neurosurgical procedures. RESULTS: In all children, ioMRI was adequate both for tumor resection control and monitoring of interventional procedures. Primary radical removal of tumor was reached in 40% as confirmed by ioMRI, but in 60% of the patients, the tumor resection procedure was extended after residual tumor was detected using the new 3D dataset for navigational update. By using ioMRI, radical tumor removal improved up to 83% as confirmed by early postoperative MRI. Procedure-related complications were not seen in our series. For all MR-guided biopsies, histology findings could be confirmed, and aspiration of intracranial cysts or abscesses could be monitored online. CONCLUSION: IoMRI using the open magnetom is suitable for detecting residual tumor tissue, can compensate for the phenomenon of brain shift using a new intraopertive 3D dataset for extended tumor resection, and is capable of monitoring interventional neurosurgical procedures. By using ioMRI for tumor resection control, the degree of tumor resection could be significantly improved.

Supratentorial malignant ependymoma in childhood: 16 years without relapse after hemispherectomy.

INTRODUCTION: Malignant intracranial ependymomas in childhood have a poor prognosis, supratentorial ependymomas have the poorest clinical course with a survival rate after 5 years of 45%. The most important prognostic factor in these cases is a radical operation, which cannot usually, however, prevent relapse. CASE REPORT: We demonstrate the case of a large malignant ependymoma of the left cerebral hemisphere in a child who has so far lived for 16 years without relapse after an extensive but uncomplicated left-sided hemispherectomy. The patient has also shown an improvement in her preoperative neurologic deficits. Her epilepsy, which was difficult to manage preoperatively, has been completely eliminated. She went to a special school for handicapped children and now works there. She does not need any help in handling everyday activities. CONCLUSION: This case shows the significance of complete tumor resection in malignant ependymomas, which may, under certain circumstances, lead to lasting tumor control.

Acute haemorrhage into a microcystic meningioma leading to cerebral herniation.

Low-grade (WHO level I) meningiomas are slow-growing, benign tumours typically presenting with unspecific symptoms (e.g. headache), seizures, cranial nerve compression and neuropsychological symptoms determined by location and size of the lesion. Haemorrhagic onset and sequelae are rare, and have been described infrequently. This is a case of a 50-year-old male presenting with signs of tentorial herniation secondary to hyperacute intratumoural haemorrhage (ITH) into a previously undiagnosed meningioma. Emergency surgical decompression and exstirpation of the lesion helped to achieve a favourable outcome. ITH has been described in all including benign intracranial neoplasms. Factors associated with a higher risk for haemorrhage in meningiomas are discussed. Though haemorrhages associated with meningiomas have been reported, ITH into low-grade meningiomas leading to herniation remains a rarity. Bearers of known lesions and their treating physicians who opt for conservative or delayed treatment should be aware of this remote complication.

Expression and immunolocalization of the multidrug resistance proteins, MRP1-MRP6 (ABCC1-ABCC6), in human brain.

Multidrug resistance proteins (MRPs, symbol ABCC) are membrane glycoproteins that mediate the ATP-dependent export of organic anions, including cytotoxic and antiviral drugs, from cells. To identify MRP family members possibly involved in the intrinsic resistance of human brain to cytotoxic and antiviral drugs, we analyzed the expression and localization of MRP1-MRP6 in rapidly frozen perilesional samples of several regions of adult human brain obtained during neurosurgery. Quantitative polymerase chain reaction analysis showed expression of MRP1, MRP2, MRP3, MRP4, and MRP5 mRNA, whereas MRP6 mRNA was below detectability. However, immunofluorescence microscopy of cryosections from human brain showed no reactivity for the MRP2 or MRP3 proteins. The proteins MRP1, MRP4, and MRP5 were clearly localized by confocal laser scanning microscopy to the luminal side of brain capillary endothelial cells. The MRP4 and MRP5 proteins were also detected in astrocytes of the subcortical white matter. Notably, MRP5 protein was present in pyramidal neurons. MRP proteins may, thus, contribute to the cellular efflux of endogenous anionic glutathione or glucuronate conjugates (substrates for MRP1), cyclic nucleotides (substrates for MRP4 and MRP5), or glutathione (co-substrate for MRP1 and MRP4); in addition, they may play an important role in the resistance of the brain to several cytotoxic and antiviral drugs.

Cell death induction by betulinic acid, ceramide and TRAIL in primary glioblastoma multiforme cells.

BACKGROUND: Glioblastoma multiforme (WHO Grade IV, GBM) is the most malignant brain tumour with a mean survival time of less than one year. Betulinic acid, ceramide and TRAIL (TNF-related apoptosis inducing ligand) represent novel therapeutic agents for potential use in GBM. METHOD: Primary GBM cells of 21 patients with macroscopically complete tumour resection were tested in vitro for cell death induction by betulinic acid, ceramide, TRAIL and established therapeutics (BCNU, cisplatin, doxorubicin, vincristin and gamma-irradiation). FINDINGS: At peak plasma concentrations (PPC), Betulinic acid, ceramide and TRAIL induced cell death in primary GBM cells at higher rates than established cytotoxic drugs. Specific cell death > or =75% was observed in 43% (9/21), 38% (8/21), and 19% (4/21) for betulinic acid, ceramide, and TRAIL respectively, while this was only found in 5% (1/21) of gamma-irradiated and cisplatin-treated cells, and in none of the GBM cultures, where BCNU or vincristin were applied in PPC. CONCLUSION: Due to a markedly improved cell death of GBM cells as compared with established therapeutics, Betulinic acid, ceramide and TRAIL might represent potent substances for future treatment of GBM.

Low frequency of chromosomal imbalances in anaplastic ependymomas as detected by comparative genomic hybridization.

We screened 26 ependymomas in 22 patients (7 WHO grade I, myxopapillary, myE; 6 WHO grade II, E; 13 WHO grade III, anaplastic, aE) using comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). 25 out of 26 tumors showed chromosomal imbalances on CGH analysis. The chromosomal region most frequently affected by losses of genomic material clustered on 13q (9/26). 6/7 myE showed a loss on 13q14-q31. Other chromosomes affected by genomic losses were 6q (5/26), 4q (5/26), 10 (5/26), and 2q (4/26). The most consistent chromosomal abnormality in ependymomas so far reported, is monosomy 22 or structural abnormality 22q, identified in approximately one third of Giemsa-banded cases with abnormal karyotypes. Using FISH, loss or monosomy 22q was detected in small subpopulations of tumor cells in 36% of cases. The most frequent gains involved chromosome arms 17 (8/26), 9q (7/26), 20q (7/26), and 22q (6/26). Gains on 1q were found exclusively in pediatric ependymomas (5/10). Using FISH, MYCN proto-oncogene DNA amplifications mapped to 2p23-p24 were found in 2 spinal ependymomas of adults. On average, myE demonstrated 9.14, E 5.33, and aE 1.77 gains and/or losses on different chromosomes per tumor using CGH. Thus, and quite paradoxically, in ependymomas, a high frequency of imbalanced chromosomal regions as revealed by CGH does not indicate a high WHO grade of the tumor but is more frequent in grade I tumors.

[Functional capacity after peripheral nerve lesion: significance of pain syndromes]. / Begutachtung peripherer Nervenschäden. Wertigkeit von Schmerzsyndromen.

INTRODUCTION: The loss of functional capacity by peripheral nerve lesion is easy to be estimated: A certain neurologic dysfunction results in a characteristic reduction of the former individual capacity. In contrast, the effect of accompanying pain to every-day life and working ability is not known exactly. In this study, we compared the results of judgement in nerve lesions under the circumstances of additional pain syndromes. METHODS: From January 1994 until December 1998 we saw 57 patients with peripheral nerve lesions, part of them with an additional pain syndrome. Beside conventional neurological examination a detailed pain analysis has been done. RESULTS: Lesions of the median or ulnar nerves showed regularly disturbances in neurological functions (10/14 for the median nerve, 13/16 for the ulnar nerve). Astonishing is the fact, that serious pain after nerve lesion only occurs in cases of partial nerve lesion. We saw neuralgias in 6 patients with ulnar neuropathy, in three cases of median nerve lesions we could see severe neuralgia (causalgia we found in 3 cases of ulnar neuropathy, in 6 cases after Median Nerve lesion). Patients with a lesion of the central plexus brachialis showed in 10 of 11 cases an additional pain syndrome. Other nerves have been affected more rarely. For the judgement of the loss of earning capacity we saw an additional pain related diminuition of at least 10% compared to those patients without pain problems. CONCLUSIONS: The common grading scales for peripheral nerve lesions are not suitable in cases accompanied by an additional pain syndrome. Beside a functional deficit the effect of severe pain in these patients has to be estimated. On an average, patients with additional pain-problems get a 10% extended loss of earning capacity, even more in particular cases.

Autocrine growth regulation by granulocyte colony-stimulating factor and granulocyte macrophage colony-stimulating factor in human gliomas with tumor progression.

Granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) and/or their receptors are increasingly detected in solid human tumors, although little is known about their function in tumor growth and invasion. We analyzed RNA and protein expression of both factors and their receptors in 22 human gliomas (WHO grade II, III, and IV) and derived cell cultures. G-CSF, GM-CSF, and/or their receptors were expressed in all tumors and derived cell cultures, but coexpression of both factors and receptors was almost exclusively found in grade IV glioblastomas and thus correlated with advanced tumor stage. The functional significance of G-CSF and GM-CSF as regulators for glioma cells was demonstrated by 1) stimulation of proliferation and migration in tumor cells expressing one or both receptors by the corresponding factor; 2) inhibition of growth and migration of glioma cells expressing G-CSF, GM-CSF, and their receptors by neutralizing antibodies to both factors. These results indicate a significant role for both factors in the autocrine regulation of growth and migration in late-stage malignant gliomas and suggest a shift from paracrine to autocrine regulation with tumor progression. The implication of G-CSF and GM-CSF in glioblastoma growth regulation could make these factors further prognostic indicators and raises questions concerning their use in cancer therapy.

Betulinic acid: a new cytotoxic agent against malignant brain-tumor cells.

Malignant brain tumors are the most common solid tumors in children. The overall prognosis for this group of patients is still poor, emphasizing the importance of more effective therapies. Betulinic acid (Bet A) has been described as a novel cytotoxic compound active against melanoma and neuroblastoma cells. Here we report that Bet A was active against medulloblastoma and glioblastoma cell lines. In addition, Bet A exerted cytotoxic activity against primary tumor cells cultured from patients in 4 of 4 medulloblastoma-tumor samples tested and in 20 of 24 glioblastoma-tumor samples. Since a small percentage of primary-glioblastoma-tumor cells (4/24) did not respond to Bet-A treatment, resistance to Bet A might occur. Induction of apoptosis by Bet A involved mitochondrial perturbations, since inhibition of the mitochondrial permeability transition by the mitochondrion-specific inhibitor bongkrekic acid (BA) reduced Bet-A-induced apoptosis. In addition, mitochondria undergoing Bet-A-induced permeability transition triggered DNA fragmentation in isolated nuclei. Cytochrome c was released from mitochondria of Bet-A-treated cells, and might be involved in activation of caspases. Following treatment with Bet A, caspase-8, caspase-3 and PARP were proteolytically processed. Inhibition of caspase cleavage by the broad-range caspase inhibitor zVAD.fmk strongly reduced Bet-A-induced apoptosis, indicating that apoptosis was mediated by activation of caspases. Since Bet A did not exhibit cytotoxicity against murine neuronal cells in vitro, these findings suggest that Bet A may be a promising new agent for the treatment of medulloblastoma and glioblastoma cells that clearly warrants further pre-clinical and clinical evaluation.

[Fibrinolysis of intraventricular hematoma with rt-PA]. / Fibrinolyse intraventrikulärer Hämatome mit rt-PA.

Intraventricular administration of recombinant tissue plasminogen activator (rt-PA) is an experimental therapy to hasten the lysis of intraventricular hemorrhages. We report nine patients (7 male, 2 female, mean age 64a) with intracerebral hematoma with ventricular extension who were treated with intraventricular infusion of rt-PA (2-32 mg, mean dose 17 mg). In two patients, clinically significant bleeding complications were associated with the fibrinolytic therapy. In one of these patients, fibrinolytic therapy was stopped. Other complications could not be observed. In eight of all nine patients, a rapid and extensive reduction of the amount of intraventricular blood occurred. A persistent shunt became necessary in two patients. We conclude, that intraventricular fibrinolysis probably leads to a faster clearance of intraventricular blood. Despite of fibrinolytic treatment, a permanent shunt becomes necessary in some cases. Intraventricular fibrinolysis is a potentially hazardous therapy with the risks of bleeding complications and infection.

Expression and functional significance of vascular endothelial growth factor receptors in human tumor cells.

Vascular endothelial growth factor (VEGF) is one of the key factors in tumor neoangiogenesis, acting through its receptors KDR (VEGFR-2) and fit-1 (VEGFR-1) expressed on endothelial cells. Our data demonstrate that VEGFR-1 and to a lesser extent VEGFR-2 are expressed in a number of human tumor tissues and derived cells in culture. VEGFR-1 protein is expressed in 26 of 42 glioma tissues, 22 of which show a coexpression of VEGFR-1 with VEGFR-2; 1 glioma tissue expresses exclusively VEGFR-2. In the derived glioma cell cultures, we found VEGFR-1 mRNA expression in 6 of 11 cultures, with one coexpressing VEGFR-1 and VEGFR-2. Of four established glioma cell lines, two expressed VEGFR-1. In addition VEGFR-1 protein expression was demonstrated in 30 of 37 tumor tissues of squamous cell carcinomas of the head and neck, with VEGFR-2 coexpression in 15 tissues and an expression of VEGFR-2 alone in 1 tissue. Derived tumor cell cultures showed mRNA expression of VEGFR-1 alone in seven of seven cases. Established melanoma cell lines expressed VEGFR-1 mRNA in four of five lines, with VEGFR-2 coexpression in two lines. Concerning the functional significance of VEGF receptor expression, VEGF treatment of VEGFR-1-expressing tumor cells induced the inhibition of cell proliferation by 25 to 55% and the inhibition of tumor cell migration by 29 to 55%. Thus our data indicate that the coexpression of VEGF and VEGFR-1 in tumor cells could have an inhibitory effect on tumor cell proliferation and migration, a mechanism possibly induced as a response to a deficiency in nutrient and oxygen supply.

Immunization with virus-modified tumor cells.

Direct infection of tumor cells with viruses transfering protective or therapeutic genes-a frequently used procedure for production of tumor vaccines in human gene therapy-is often limited by the number of tumor cells that can reliably be infected, as well as by issues of selectivity and safety. In this review, we describe an efficient, selective, and safe way of infecting human tumor cells with a natural virus with interesting pleiotropic immune stimulatory properties, the avian paramyxovirus Newcastle disease virus (NDV). Advantages of this virus are its good cell-binding properties, its selective replication in tumor cell cytoplasm, which is independent of cell proliferation, and its relative safety. Most important for its use as an adjuvant in human cancer vaccine are its ability to introduce T-cell costimulatory activity, to prevent anergy induction, and to induce locally chemokines (eg, RANTES, IP-10) and cytokines (eg, interferon alpha, beta [IFN-alpha, beta] and tumor necrosis factor-alpha [TNFalpha]) that affect T-cell recruitment and activation. A further development consists of attachment-via NDV-derived hemagluttinin-neuraminidase (HN) membrane-anchoring molecules-of universal defined bispecific reagents such as T-cell-activating anti-CD28 antibodies. Finally, we summarize the status of our clinical studies with the autologous virus modified live cell vaccine (ATV)-NDV.

[Prognosis of brain tumors: epidemiology, survival time and clinical course]. / Zur Prognose von Hirntumoren: Epidemiologie, Uberlebenszeit und klinischer Verlauf.

Although the frequency of primary brain tumors is relatively small compared to other tumors such as breast or lung carcinoma, brain tumors affect a particularly young and healthy patient population and possess a high portion of cancer mortality in these age groups. Generally brain tumor diseases influence the professional capacity in younger people and cause significant socioeconomical costs. Prognosis and clinical deterioration of primary brain tumors are determined by histopathological diagnosis first, by tumor location and -volume second. The clinical malignancy of brain tumors, caused by histopathological findings, has not essentially been changed in the last years despite more effective therapies. In contrast refinement in technical standards and computer-assisted micro-surgery makes a valuable progress in the treatment of biological benign brain tumors. Most of these patients recover normal efficiency including former working capability. On the other hand therapeutical nihilism is not supposed to be a sufficient answer to primary brain tumors, because in selected cases a longer lasting stabilization of the disease is possible. In future only through better understanding of the biology of brain tumors and much more effective therapies we can hope to make significant progress in the treatment of these tumors.

Early hemicraniectomy in patients with complete middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Malignant, space-occupying supratentorial ischemic stroke is characterized by a mortality rate of up to 80%. Several reports indicate a beneficial effect of hemicraniectomy in this situation. However, whether and when decompressive surgery is indicated in these patients is still a matter of debate. METHODS: In an open, prospective trial we performed hemicraniectomy in 63 patients with acute complete middle cerebral artery infarction. Initial clinical presentation was assessed by the Scandinavian Stroke Scale (SSS) and the Glasgow Coma Scale (GCS). All survivors were reexamined 3 months after surgical decompression, with the clinical evaluation graded according to the Rankin Scale (RS) and Barthel Index (BI). We analyzed the influence of early decompressive surgery (<24 hours after symptom onset, based on clinical status at admission and initial CT findings) versus late surgery (>24 hours after first reversible signs of herniation) on mortality, functional outcome, and the length of time of critical care therapy was needed. RESULTS: In total, 46 patients (73%) survived. Despite complete hemispheric infarction, no survivor suffered from complete hemiplegia or was permanently wheelchair bound. In patients with speech-dominant hemispheric infarction (n=11), only mild to moderate aphasia was present. The mean BI score was 65, and RS score revealed severe handicap in 13% of the patients. In 31 patients with early decompressive surgery, mortality was 16% and BI score 68.8. Early hemicraniectomy led to a significant reduction in the length of time critical care therapy was needed (7.4 versus 13.3 days, P<0.05). CONCLUSIONS: In general, the outcome of patients treated with craniectomy in severe ischemic hemispheric infarction was surprisingly good. In addition, early decompressive surgery may further improve outcome in these patients.

Secondary hemorrhage after intraventricular fibrinolysis: a cautionary note: a report of two cases.

OBJECTIVE AND IMPORTANCE: To hasten the lysis of intraventricular hemorrhages, intraventricular administration of recombinant tissue plasminogen activator (rt-PA) or urokinase has been advocated as an effective and safe treatment for patients with intraventricular hemorrhage. Until now, cases of secondary hemorrhage after intraventricular fibrinolysis, to our knowledge, have not been reported in the literature. We present a report of two patients with clinically significant bleeding complications associated with intraventricular infusion of rt-PA. CLINICAL PRESENTATION: Both patients, a 42-year-old woman (Patient 1) and a 70-year-old man (Patient 2), suffered from hypertensive left-sided thalamic hemorrhage with ventricular extension and ventricular dilatation. INTERVENTION: Both patients required external ventricular drainage and were treated with intraventricular rt-PA. In Patient 1, a secondary intraventricular hemorrhage occurred 20 minutes after the first instillation of 2 mg of rt-PA and was associated with a sudden loss of consciousness. Treatment with rt-PA was stopped, and the patient needed a permanent shunt. In Patient 2, intraventricular subsequent bleeding was noted 4 hours after the second 4-mg dose of rt-PA, clinically apparent as anisocoria. In Patient 2, rt-PA administration was continued without further complications. In both patients, a second external ventricular drainage was required after secondary hemorrhage. CONCLUSION: Intraventricular lysis is a potentially hazardous therapy. To weigh the potential benefits against the potential risks, a controlled study of this promising new treatment is urgently warranted.

Hemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction.

Surgical decompression to alleviate raised intracranial pressure has been reported repeatedly in the past decades in small series of patients. Only recently have there been indications from larger trials that surgical decompression may be beneficial in treating space-occupying hemispheric infarction. However, surgical requirements for the procedure to be effective have not yet been defined. Based on theoretical criteria, the authors operated on 43 patients with medically uncontrollable hemispheric infarctions. The craniectomies were planned to be as large as possible and performed in combination with a subtemporal decompression. Postoperative computerized tomography scans were evaluated for these criteria. The mean survival rate for the group of 43 patients was 72.1% and no surviving patient ended up in a vegetative state. The mean area of craniectomy was found to be 84.3 +/- 16.5 cm2 and the mean distance of the inferior craniectomy margin to the middle fossa was 1.8 +/- 1.3 cm. Comparison of survivors and nonsurvivors failed to show a significant difference in the size of craniectomy or the distance to the floor of the middle fossa. Compared with the reported 80% fatality rate for medically treated stroke patients, in this subgroup the outcome (72.1% survival rate) is remarkably good. The authors conclude that decompressive craniectomy is an effective treatment, able to reduce mortality, and to improve neurological outcome in patients with space-occupying cerebral infarction if the size of craniectomy is large enough. Nevertheless, there is a need for further investigation to identify patients who will benefit from surgery and predictors to optimize the timing of surgical intervention.

[Brain metastases in renal cell carcinoma. Results of treatment and prognosis]. / Hirnmetastasierung beim Nierenzellkarzinom. Behandlungsergebnisse und Prognose.

Brain metastases develop as a late manifestation of renal cell cancer (RCC) and pose an increasing challenge to urologists as a result of the more frequent prolonged survival of patients with advanced RCC. Therapeutic options, including surgical resection and radiotherapy, were analyzed retrospectively to assess survival and to identify factors influencing prognosis in a group of 90 patients treated either by brain metastasectomy (n = 64) or radiotherapy (n = 26). The analysis confirmed that the overall median survival was a disappointing 461 days and the 1-year survival rate was 31% for patients treated by surgical resection and 310 days and 15% respectively for patients treated by radiotherapy. However, a subgroup of patients who, benefitted significantly from aggressive treatment of metastases could be defined. The following favorable prognostic factors showed a trend toward improved survival: (1) metachronous appearance of brain metastases more than 1 year after nephrectomy (P < 0.0001), (2) good patient performance (Karnofsky > 70) (P < 0.0002), (3) patient's age under 50 years (P < 0.05), (4) solitary lesions (P < 0.05), (5) minimal or no neurological deficit (P < 0.05), and (6) the absence of/or minimal extracranial metastases (P < 0.05). No influence of lesion size and localization (infratentorial vs supratentorial) on survival was detected. Surgical treatment of recurrent brain tumors (n = 17) yielded and additional median survival advantage of 8 months as compared to untreated patients (n = 16). Our results suggest that, especially in patients with good prognostic criteria, a radical metastasectomy plus vigorous surgery of local recurrences and, if required, subsequent systemic immuno- or chemoimmunotherapy should be performed. In patients with poor prognosis, stereotactic radiosurgery is recommended for palliation and survival prolongation.

Craniectomy: an aggressive treatment approach in severe encephalitis.

BACKGROUND AND OBJECTIVE: Focal encephalitis may be associated with brain edema, which is often fatal. The control of intracranial pressure (ICP) is therefore crucial for further therapeutic strategies in space-occupying edema following encephalitis. However, aggressive treatment strategies such as hemicraniectomy have not been described in a larger series of patients. PATIENTS AND METHODS: We describe the clinical course and outcome in six patients who developed severe brain edema associated with acute encephalitis. All received maximum medical treatment for elevated ICP, but with signs of brainstem compression emerging, hemicraniectomy was performed to control ICP. RESULTS: All patients had a very severe encephalitic syndrome and were treated over the course of weeks in the neurocritical care unit (NCCU). However, all patients recovered almost completely and showed only mild or no neurologic deficit when reexamined after 4 months to 3 years. CONCLUSIONS: Hemicraniectomy should be considered in patients with severe brain edema following encephalitis as a potentially lifesaving therapeutic measure. Moreover, the initial neurologic deficit seems to have no impact on the long-term clinical outcome.

Entrapment neuropathy at the cubital tunnel: simple decompression is the method of choice.

We present a retrospective study of 41 patients treated by simple decompression for ulnar neuropathy. Pre- and postoperatively, patients were evaluated clinically and electrophysiologically. The median follow-up was 2 years (minimum: 0.5 years, maximum: 5.1 years). The leading pre-operative sign was motor loss in the ulnar distribution (36 patients = 89%) with consecutive atrophy of ulnar innervated muscles (30 patients = 75%). The secondary complaint was sensory impairment in 59% of all cases, less frequently patients presented with pain or paraesthesia. In the majority of cases the aetiology remained unknown (27 patients = 65%). When aetiology was known, previous trauma to the elbow was reported most frequently (9 patients = 22%). Motor nerve conduction velocity (mNCV), compared to the contralateral, non-involved arm, was lower at least for 10 m/s. In cases with atrophy of the ulnar innervated muscles the difference was greater than 15 m/s. In 89%, postoperative results were good or even very good. In 8% (3 patients) no improvement was observed. Worsening due to surgery did not occur. We could demonstrate a significant increase in postoperative mNCV of 7.95 m/s in all patients (p < 0.05). There is still disagreement as to the correct surgical treatment of this disorder. We favour simple decompression (SD) as the appropriate operative technique for cubital tunnel syndrome.