Complete resection of a cavernous haemangioma of the optic nerve, the chiasm, and the optic tract.

The involvement of the optic nerve, the chiasma, and the optic tract by a cavernoma has been reported in only three patients. In all of them, a biopsy of the vascular lesion was obtained. We report a further example of a 38-year-old male patient who suffered from acute onset of severe headache and progressive loss of vision. The vascular malformation of the optic pathways was completely removed via a pterional approach. This is the first reported instance of complete resection of a cavernoma involving the optic nerve, the chiasm, and the optic tract.

Study of clinical features of amyloid angiopathy hemorrhage and hypertensive intracerebral hemorrhage.

OBJECTIVE: The purpose of this study was to differentiate between cerebral amyloid angiopathy (CAA) and hypertension (HTN) based on hemorrhage pattern interpretation. METHODS: From June 1994 to Oct., 2000, 83 patients admitted to our service with acute intracerebral hemorrhage (ICH) were investigated retrospectively; 41 patients with histologically proven diagnosis of cerebral amyloid angiography and 42 patients with clear history of hypertension were investigated. RESULTS: Patients with a CAA-related ICH were significantly older than patients with a HTN-related ICH (74.0 years vs 66.5 years, P < 0.05). There was a significantly higher number of hematomas > or = 30 ml in CAA (85.3%) when compared with HTN (59.5%). No basal ganglional hemorrhage was seen in CAA, but in 40.5% in HTN. In CAA-related ICH, subarachnoid hemorrhage (SAH) was seen in 26 patients (63.4%) compared to only 11 patients (26.2%) in HTN-related ICH. Intraventricular hemorrhage was seen in 24.4% in CAA, and in 26.2% in HTN. Typical features of CAA-related ICH included lobar distribution affecting mainly the lobar superficial areas, lobulated appearance, rupture into the subarachnoid space, and secondary IVH from the lobar hemorrhage. More specifically, multiplicity of hemorrhage, bilaterality, and repeated episodes also strongly suggest the diagnosis of CAA. Multiple hemorrhages, defined as 2 or more separate hematomas in multiple lobes, accounted for 17.1% in CAA-related ICH. CONCLUSION: There are certain features in CAA on CT and MRI and in clinical settings. To some extent, these features may contribute to distinguishing CAA from HTN related ICH.

Metastatic low-grade inflammatory myofibroblastic tumor (IMT) in the central nervous system of a 29-year-old male patient.

A case of myofibrosarcoma (IMT) of the brain and lung as well as the spinal cord is described. A 29-year-old male patient presented with fever (40 degrees C), malaise, vomitus, meningism and leukocytosis. Computer tomography identified a bleeding in the left frontal lobe. A bleeding angioma was suspected and an operation was performed. The histological examination could not reveal an exact diagnosis. Eight months after complete recovery from the first bleeding, the patient had a second intracranial temporo-occipital bleeding on the right side which has been removed operatively. A new lesion was seen in the left parietal white matter of the brain. A growing cavernoma was suspected and resection of the lesion was planned. Pre-operatively the patient suffered from hemoptysis and fever. The X-ray of the chest showed a pulmonary lesion in the left lower lobe. In the CT of the chest a large tumor in the left lower lobe of the lung and additionally a cystic structure in the mediastinum was seen. The histological examination of this tumor identified an inflammatory myofibroblastic tumor (IMT). The left parietal lesion has been resected after the thoracic operation. The brain lesions were estimated to be metastases of the IMT of the lung. In the further clinical history the patient developed a large spinal cord metastasis of the thoracic spine. The metastatic development of the tumor reported in this case is unusual. The current therapy of these tumors consists of complete tumor resection and further clinical controls. However, due to the localization and the extension of some lesions in the present case, the complete resection has not been possible. There is no proven role of chemotherapy and radiation therapy. The patient died due to the pulmonary deterioration.

Outcome and prognostic factors of hemicraniectomy for space occupying cerebral infarction.

OBJECTIVE: To determine long term functional outcome and length of survival of patients undergoing decompressive craniectomy for space occupying infarction of the middle cerebral artery (MCA), and to identify risk factors associated with death and unfavourable outcomes METHODS: Databases of patients undergoing decompressive craniectomy for space occupying MCA infarction compiled at eight neurosurgical departments (1996-2001) were merged, and 188 patients were evaluated. Mortality was calculated by the Kaplan-Meier method. Clinical outcome was rated using the Glasgow outcome scale (GOS). The prognostic impact of patient related covariates on length of survival and the GOS was analysed multivariately. RESULTS: The unadjusted 3, 6, and 12 month mortality rates were 7.9%, 37.6%, and 43.8%, respectively (median follow up, 26 weeks). In the "best" multivariate model, age >50 years (p<0.02) and the involvement of two or more additional vascular territories (p<0.01) had an unfavourable impact on length of survival. The adjusted six month mortality was as low as 20.0% (no risk factor) and as high as 59.7% (two risk factors). A GOS score of 50 years (p<0.0003): 34.9% of the patients 3, as compared with 12.0% of the elderly subpopulation. The side of the infarct did not have prognostic relevance. CONCLUSIONS: Results of surgical treatment in patients <50 years of age undergoing decompressive craniectomy are encouraging. The effectiveness of decompressive craniectomy for patients >50 years remains questionable and should be analysed in the framework of a prospective randomised study.

Subarachnoid hemorrhage of unknown origin and the basilar artery configuration.

It is unclear whether the configuration of the basilar artery (BA) in patients with subarachnoid hemorrhage (SAH) of unknown origin is comparable to that in normal subjects or whether there are differences which may help to identify the origin. We studied the BA configuration in 57 patients with SAH of unknown origin (10%), who were identified in a prospectively collected series of 549 SAH patients consecutively admitted to our service over a 9-year period. There were 30 patients (53%) with non-perimesencephalic SAH and 27 with perimesencephalic SAH (47%). According to a standardized algorithm we determined, on straight anteroposterior digital subtraction angiography (DSA), the width of the proximal BA segment at the origin of the anterior inferior cerebellar artery and the width of the most distal BA segment between the superior cerebellar arteries and the posterior cerebral arteries. Based on these measurements we calculated the distal-proximal BA ratios and compared them to the ratios obtained in a control group of 31 patients who had DSA for reasons other than aneurysmal SAH. The mean ratio in patients with non-perimesencephalic SAH of unknown origin was 1.150 (range: 1.080-1.230). In patients with perimesencephalic SAH of unknown origin it was 1.156 (range: 1.120-1.250). In the control group the mean ratio was 1.163 (range: 1.125-1.200). There are no variations in the configurations of the BA which could possibly explain the cause of this type of SAH or clarify the origin of hemorrhage.

Clinical outcome after surgery of intracranial unruptured aneurysms: results of a series between 1991 and 2001.

The clinical results of surgery for unruptured aneurysms in the Neurosurgical Department of Kiel were analyzed to further discuss whether an operative treatment can be advised. Between 1991 and 2001, 54 unruptured aneurysms in 45 patients were operated in our department. No complications occurred in 38 patients; transient complications (slight aphasia, hemiparesis, psychiatric disorders) in 4 patients; postoperative seizures in one, epidural haematoma with the need of re-operation in one, and infection in another patient. At the time of discharge, GOS was 5 in 33 patients, 4 in 12 patients. But the slight disabilities were due to the aneurysm operation only in two patients, in the other 10 patients they were caused by pre-existing concomitant diseases. The Rankin-Scale after at least 6 months was 1 (no disability) in 31 patients (37 patients investigated); 2 (slight disability) in 5, and 3 (moderate disability) in one patient. In only one of these patients, the slight disability was caused by the aneurysm operation. During a telephone interview performed between 6 months and 7 years after the operation, all patients except two (31 patients investigated) gave a positive answer to the question, whether, in case of diagnosis of an aneurysm, they would undergo an operation again. Regarding our results, we still advocate treatment of unruptured aneurysms in patients who are in stable clinical conditions, especially in young patients and in patients with unique aneurysm configurations and aneurysm sizes approaching 10 mm.

Therapeutical considerations in patients with intracranial venous angiomas.

The clinical presentation of intracranial venous angiomas are usually headache, seizures or dizziness. Very often these anomalies are found incidentally on magnetic resonance imaging (MRI). We reviewed 35 patients, which were examined in our department between 1994 and 2000. Only one patient became symptomatic with an intracranial haematoma, which was removed surgically. In three patients an associated cavernous angioma was found, which was removed successfully with preservation of the coexisting venous angioma. There is no indication in operating a venous angioma because the risk of postoperative deterioration caused by venous infarction is high. When removing cavernous angiomas the associated venous angioma has to be preserved.

Role of potassium channels in the relaxation induced by the nitric oxide (NO) donor DEA/NO in the isolated rat basilar artery.

This study investigates whether potassium ion (K+) channels are involved in the nitric oxide (NO)-induced relaxation in segments of the isolated rat basilar artery, mounted onto a wire myograph. A high extracellular K+ concentration partly inhibited the relaxant effects of the NO donors DEA/NO and SIN-1 (3-morpholino-sydnonimine). Whereas single applications of the K+ channel inhibitors tetraethyl-ammonium (10(-3) M), glibenclamide (10(-6) M), 4-aminopyridine (10(-3) M), or BaCl(2) (5 x 10(-5) M) did not affect the responses to DEA/NO, a combination of these inhibitors reduced the effects of DEA/NO. These data suggest, that the relaxant effects of NO donors are partly mediated via activation of K+channels. Different K+ channel types seem to be involved that function in a redundant manner and compensate for each other.

Stroke pattern interpretation: the variability of hypertensive versus amyloid angiopathy hemorrhage.

INTRODUCTION: It is commonly felt that cerebral amyloid angiopathy (CAA) related intracerebral hemorrhage (ICH) can be distinguished from hypertension (HTN)-related ICH by certain typical features on computerized tomography (CT) and magnetic resonance imaging (MRI). The purpose of this study was to investigate the performance of clinicians who were asked to differentiate between CAA and HTN based on hemorrhage pattern interpretation and to assess the feasibility of such classification. METHODS: The admission scans from 83 patients who were admitted to our service with an acute ICH were presented to 5 clinicians in a randomized and blinded fashion (1 junior, and 1 senior neurosurgical resident, 1 attending neurosurgeon, and 2 neurosurgeon-neuroradiologists). There were no patients who received oral anticoagulants other than low-dose aspirin, or who suffered from vascular malformations or tumors. Scans from 41 patients with a histologically proven diagnosis of CAA and from 42 patients with a clear history of HTN were investigated. Hematoma evacuation was done in all CAA patients and in 59% of HTN patients (n = 25). RESULTS: The overall average classification accuracy was 66.8% (range: 62.7-69.9). For correct HTN classification it was 69.5% (range: 64.3-81), and 63.9% for CAA, respectively (range: 48.9-75.6). There were negligible differences in classification accuracy among all observers. Patients with a CAA-related ICH were significantly older than patients with a HTN-related ICH (74 vs. 66.5 years, p < 0.05). There was a significantly higher number of hematomas >30 ml in CAA (85.3%) when compared with HTN (59.5%). No basal ganglionic hemorrhage was seen in CAA, but in 40.5% in HTN. Intraventricular hemorrhage was seen in 24.4% in CAA, and in 26.2% in HTN. Two patients (4.9%) with CAA, and 7 patients with HTN (16.7%) presented with cerebellar hematomas. CONCLUSIONS: Three of 10 scans were not correctly diagnosed regardless of the examiner's level of training. This calls into question the reliability of classifying the underlying pathological condition based on hemorrhage pattern interpretation on CT or MRI. The definite diagnosis of CAA- versus HTN-related hemorrhage requires a histopathological confirmation and should not be based solely on hemorrhage pattern interpretation.

Granular-cell tumour: a rare suprasellar mass.

Granular-cell tumour is a rare suprasellar space occupying lesion, which usually presents with visual deterioration, endocrine deficits or headache. We present two women with extraordinarily large tumours, measuring 3.8 and 4.0 cm in diameter. In both cases the tough, vascular tumour could be removed only subtotally.

Effects of potassium channel inhibitors on the relaxation induced by the nitric oxide donor diethylamine nitric oxide in isolated human cerebral arteries.

OBJECT: The goal of this study was to investigate whether K+ channels are involved in nitric oxide (NO)-induced relaxation of isolated human cerebral arteries. METHODS: Successive concentration-response curves relating to the use of the NO donor diethylamine NO (DEA/NO) were established in the absence and presence of different K+ channel inhibitors after mounting human cerebral arteries onto a wire myograph. The arteries were obtained from macroscopically intact tissue that had been removed during brain tumor operations. A high K+ concentration partially inhibited the relaxant effects of DEA/NO. Different K+ channel inhibitors (tetraethylammonium [TEA], 10(-3) M; charybdotoxin, 10(-7) M; glibenclamide, 10(-6) M; 4-aminopyridine [4-AP], 10(-3) M; BaCl2, 5 x 10(-5) M; and apamin, 10(-6) M) alone failed to affect the responses to DEA/NO. However, a combination of TEA, glibenclamide, 4-AP, and BaCl2 partially blocked the relaxant effects of DEA/NO. In addition, the effects of DEA/NO were inhibited by the thromboxane A2 analog U46619 (3 x 10(-7) M). CONCLUSIONS: Inhibitors of the large-conductance or small-conductance Ca++-activated K+ channels, the adenosine triphosphate-sensitive K+ channels, and the delayed-rectifier or inward-rectifier K+ channels failed to alter the effects of DEA/NO when only one K+ channel blocker was used. However, a regimen of a combination of K+ channel blockers that possess selectivity for different channels demonstrated that different K+ channel types are involved; these channels may function in a redundant manner and compensate for each other. Selective thromboxane A2 agonists are capable of inhibiting the relaxant response to the NO donor.

Threshold concentrations of endothelin-1: the effects on contractions induced by 5-hydroxytryptamine in isolated rat cerebral and mesenteric arteries.

This study compares the effects of threshold concentrations of endothelin-1 in isolated rat basilar arteries with those in mesenteric arterial branches and investigates the mechanisms of inhibitory and potentiating endothelin-1-effects. In basilar arteries, endothelin-1 reduces the contractions induced by 5-hydroxytryptamine (5-HT), by the thromboxane A2 agonist U46619, and by vasopressin. The inhibitory effect of endothelin-1 on the contraction induced by 5-HT is abolished by deendothelialization, by the endothelin ET(B) receptor antagonist RES 701-1, by indomethacin, or by glibenclamide. In mesenteric arteries, endothelin-1 potentiates the contractile effects of 5-HT, U46619, and vasopressin. The potentiation of the contractile effect induced by 5-HT is only somewhat modified by deendothelialization, but abolished by the thromboxane A2 receptor antagonists GR32191 and ridogrel. U46619 potentiates the 5-HT-effect in mesenteric arteries. Thus, though the contractile endothelin ET(A) receptors were not blocked, threshold concentrations of endothelin-1 inhibited contractile effects in the rat basilar artery via activation of endothelial ET(B) receptors. Prostaglandins and ATP-sensitive K+ channels are involved in this inhibitory action. In contrast, endothelin-1 potentiates contractile actions in mesenteric arteries via the release of endogeneous thromboxane A2 from non-endothelial cells. The study points out the completely different role of the endothelium in combined effects of endothelin-1 between cerebral and mesenteric arteries.

Contractions induced by NO synthase inhibition in isolated rat basilar artery: role of the endothelium and endogenous vasoconstrictors.

Alterations of the endothelium may play a role in the generation of cerebral vasospasm. The objective of this study was to investigate the involvement of the endothelium and of endogenous endothelin (ET) on the NG-nitro-L-arginine (L-NOARG)-induced contractions in isolated rat basilar arteries. L-NOARG, NG-nitro-L-arginine methyl esther, and methylene blue, but not D-NOARG, induced concentration-dependent contractions and spontaneous vasomotion. The effect of L-NOARG was reversed by L-arginine and submaximally reduced in de-endothelialized arteries. The contractile effect of L-NOARG was completely suppressed by the ET-antagonists BQ 123 and Ro 46-2005 in a part of the basilar arteries. After washout of the respective antagonist, the L-NOARG-induced contraction started, but was not influenced by a second application of the antagonist. In another part of preparations the antagonists failed to influence the L-NOARG-induced contraction. Inconsistent suppressor effects were also observed after preincubation with ketanserin, Manning compound, losartan, or indomethacin. None of these antagonists reversed the established L-NOARG-induced contraction. Thus, endothelium-derived NO suppresses spontaneous contraction and vasomotion in rat basilar arteries. Endogenous ET, 5-HT, vasopressin, angiotensin or cyclooxygenase metabolites do not cause the contraction induced by inhibition of the NO synthase, but may act as 'trigger factors', that may play a role in rat models of cerebral vasospasm or infarction.

Interactions between vasoconstrictors in isolated human cerebral arteries.

This study investigates whether different endogeneous vasoconstrictors exert synergistic effects in isolated human cerebral arteries, because potentiation of contractile effects may play a role in the pathogenesis of cerebral vasospasm. Isolated human pial arteries obtained from macroscopically intact tissue during brain tumour operations were mounted onto a wire myograph. Concentration-response curves of 5-hydroxytryptamine (5-HT) were constructed in the absence and presence of threshold concentrations of the thromboxane A2 (TXA)-analog U46619, and endothelin-1 (ET-1). Threshold concentrations of U46619 markedly enhanced the maximum contractile effect of 5-HT. The response to 5-HT remained markedly increased even after washout of U46619. Threshold concentrations of ET-1 increased the maximum response to 5-HT, and markedly shifted the dose-response curve to the left. Even after washout of ET-1, the dose-response curve of 5-HT remained shifted to the left. The increase of the contractile effect of 5-HT in the presence of U46619 did not correlate with the relaxant action of the endothelium-dependent vasodilator carbachol. Thus, synergism between contractile substances such as 5-HT, U46619, or ET-1 is seen in human cerebral arteries, and responses to 5-HT are potentiated even after washout of ET-1 and U46619. The potentiation does not depend on the endothelial function. We conclude that synergistic responses between endogeneous vasoconstrictors such as 5-HT, TXA and ET-1 may be involved in the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage.

Effects of potassium channel openers in isolated human cerebral arteries.

The objective of this study was to compare the relaxant effects of the K+ channel openers pinacidil and lemakalim in isolated human pial arteries with the effects of the dihydropyridines nifedipine and nimodipine and the prostacyclin analog iloprost. Relaxation was measured in vessels contracted by 40 mmol/L K+. In contrast to the potent and consistent relaxant effects of nifedipine, nimodipine, and iloprost, the potency of pinacidil and lemakalim proved to be highly variable and inversely correlated with the onset velocity of the preceding contractions of K+ as well as with the endothelium-dependent relaxation of carbachol. Thus, in contrast to dihydropyridines and iloprost, pinacidil and lemakalim selectively elicited potent relaxations in those arteries that exhibited signs of altered vascular wall functions.

Quinidine-induced potentiation of cardiovascular effects of nitrendipine: functional aspects and possible molecular mechanisms.

The functional interaction between the dihydropyridine calcium channel blocker nitrendipine and quinidine was studied in isolated preparations from guinea-pig cardiac ventricle and in mesenteric arterial segments under a variety of experimental conditions. The negative inotropic potency of nitrendipine is clearly enhanced by quinidine (3 x 10(-6)-10(-4) mol/l) by up to two orders of magnitude, i.e. cardiac nitrendipine effects are potentiated. Vasorelaxant effects, however, remain largely unaffected (nitrendipine potency is increased by half an order of magnitude maximally). To elucidate the mechanism of this interaction, the ability of quinidine to potentiate the negative inotropic effect of a series of 12 dihydropyridines was compared with their voltage-dependence of action in guinea-pig left atria. No significant correlation is found (r = 0.18). Furthermore, quinidine inhibits rather than stimulates binding of tritiated nitrendipine, nimodipine or (S)-isradipine to isolated cardiac membranes. Therefore, the mechanism of the quinidine-nitrendipine interaction differs from those previously proposed for modulation of dihydropyridine binding by other drugs. We hypothesize that quinidine-occupied calcium channels adopt an intermediate affinity for nitrendipine, higher than in resting channels, but lower than the high affinity present with inactivated channels. Model calculations which are based on this assumption are able to reproduce all experimental findings of this study.

Non-synergistic relaxant effects of vasoactive intestinal polypeptide and SIN-1 in human isolated cavernous artery and corpus cavernosum.

Since vasoactive intestinal peptide (VIP) and nitric oxide (NO) are considered to be non-adrenergic, non-cholinergic (NANC) inhibitory mediators in human penile erectile tissue, the goal of this study was to discover possible synergistic effects of exogeneous VIP and the NO donor 3-morpholino-sydnonimine (SIN-1) in human isolated cavernous arteries and cavernosal smooth muscle. In contrast to VIP, SIN-1 elicited complete and reproducible relaxant actions. Combined administration of VIP and SIN-1 revealed non-synergistic, independent relaxant effects in both investigated tissues. The results do not favour a combined administration of VIP and SIN-1 as a new therapeutic approach in the treatment of erectile dysfunction.

Endothelium-dependent noradrenaline-induced relaxation of rat isolated cerebral arteries: pharmacological characterization of receptor subtypes involved.

1. The endothelium-dependence of catecholamine-induced relaxation of rat cerebral arteries was investigated in vitro. 2. In the basilar artery (BA), the maximal relaxant response was most pronounced with noradrenaline (NA), less with isoprenaline (Iso), and only very little with terbutaline. Methoxamine and the alpha 2-adrenoceptor selective agonists BHT 933 and clonidine, had no relaxant effect. 3. In BA, the relaxation by NA or Iso was markedly attenuated by N omega-nitro-L-arginine (L-NOARG) 10(-4) M. Short term perfusion of the vessels by Triton X 100 (1:1,000) suppressed the NA-induced relaxation. 4. The relaxation induced by NA or Iso was markedly reduced in presence of L-NOARG in the posterior, medial and anterior cerebral artery. 5. In BA, NA-induced relaxation was non-competitively inhibited by propranolol, atenolol, and the beta 1- and beta 2-adrenoceptor selective antagonists, CGP 20712 A and ICI 118551. 6. The relaxant NA-effect was not affected by prazosin but was non-competitively blocked by phentolamine. 7. The Iso-induced relaxation was competitively blocked by propranolol, whereas atenolol, CGP 20712 A and ICI 118551 caused a non-competitive inhibition. 8. The experiments indicate that the catecholamine-induced relaxation in rat isolated cerebral arteries depends upon the endothelium. They suggest that the NA-induced relaxation of BA is mediated by different alpha- and beta-adrenoceptors and that the Iso-induced relaxation is mediated by different beta-receptors. The findings would also be compatible with the idea of a receptor type which cannot be characterized by the pharmacological tools that we have used.