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Elderly patients generally experience less favorable outcomes and higher mortality after acute stroke than younger patients. The aim of this study was to analyze the influence of age on outcome and safety after endovascular therapy in a large cohort of patients aged between 20 and 90 years. We prospectively acquired data of 1,000 stroke patients treated with endovascular therapy at a single center. Logistic regression analysis was performed to determine predictors of outcome and linear regression analysis to evaluate the association of age and outcome after 3 months. Younger age was an independent predictor of favorable outcome (OR 0.954, p < 0.001) and survival (OR 0.947, p < 0.001) in multivariate regression analysis. There was a linear relationship between age and outcome. Ever increase in 26 years of age was associated with an increase in the modified Rankin Scale of 1 point (p < 0.001). However, increasing age was not a risk factor for symptomatic (p = 0.086) or asymptomatic (p = 0.674) intracerebral hemorrhage and did not influence recanalization success (p = 0.674). Advancing age was associated with a decline of favorable outcomes and survival after endovascular therapy. This decline was linear from age 20 to 90 years, but was not related to lower recanalization rates or higher bleeding risk in the elderly. The efficacy of endovascular stroke therapy seems to be preserved also in the elderly and other factors than efficacy of endovascular therapy such as decreased plasticity are likely to explain the worse outcome with advancing age.

The aim of the study was to assess the influence of white matter lesions in patients with acute ischemic stroke treated with intra-arterial thrombolysis (IAT). From September 2003 to January 2010, we treated 400 patients with IAT at our institution. Of these patients, 292 were evaluated with MRI scans and included in this observational study. Clinical data were collected prospectively. Outcome after 3 months was measured with the modified Rankin Scale (mRS); mRS 0-1 was considered as favorable outcome. White matter lesions were scored visually by two observers using the semiquantitative Scheltens and Fazekas scores. Logistic regression analysis was used to identify the association of white matter lesions and clinical outcome, recanalization, and cerebral hemorrhage. The severity of white matter lesions was inversely correlated with favorable outcome, survival and successful recanalization. White matter lesions were an independent predictor of outcome (OR 0.569, p = 0.007) and survival (OR 0.550, p = 0.018) and a weak but independent predictor for recanalization (OR 0.949, p = 0.038). Asymptomatic intracerebral bleeding after IAT was associated with white matter lesions in the basal ganglia in the univariate analysis (p = 0.036), but not after multivariable analysis. The severity of white matter lesions independently predicts clinical outcome and survival in patients treated with IAT. White matter lesions are also a weak but independent predictor for recanalization. Symptomatic intracranial bleeding after IAT are not associated with white matter lesions. Therefore, white matter lesions should not be considered as a contraindication against IAT.

Background: In selected stroke centers intra-arterial thrombolysis (IAT) is used for the treatment of acute stroke patients presenting within 6 hours of symptom onset. However, data about eligibility of acute stroke patients for IAT in clinical practice are very scarce., Methods: We collected prospectively data on indications advising for or against IAT of 230 consecutive stroke patients in a tertiary stroke center., Results: 76 patients (33.0%) presented within 3 hours, 69 (30%) between 3 and 6 hours of symptom onset and 85 (37%) later than 6 hours. Arteriography was performed in 71 patients (31%) and IAT in 46 (20%). In 11 patients no or only peripheral branch occlusions were seen on arteriography and therefore IAT was not performed. In 9 patients the ICA was occluded and barred IAT and in five anatomical or technical difficulties made IAT impossible. 72 patients presenting within 6 hours did not undergo arteriography and thrombolysis, mostly because of mild (n=44) or rapidly improving neurological deficits (n=13). Other reasons to withhold IAT were CT and/or clinical findings suggesting lacunar stroke due to small vessel occlusion (n=7), limiting comorbidty (n=7) and baseline international normalized ratio>1.7 (n=1)., Conclusions: A third of the patients underwent diagnostic arteriography and one fifth received IAT. The most important reasons to withhold thrombolysis were presentation beyond the 6 hours time window and mild or rapidly improving symptoms.

Objectives: To establish an adequate definition of acute disseminated encephalomyelitis (ADEM) in adults, based on our clinical observations of a case-series., Methods: Over a period of three years 10 adult patients with a para- or postinfectious disseminated (diffuse or multifocal) syndrome of the CNS fulfilling predefined strict criteria for the diagnosis of ADEM were encountered and systematically followed., Results: The age ranged from 21 to 62 years, two were men. MRI was normal in 5 patients and only mildly abnormal in the remaining patients. CSF was normal in 5 patients and mildly abnormal in the remainder, EEG was abnormal in 7/8 patients. All patients survived and were followed over a period of 30 months (range: 8 to 48 months). Nine patients were left with some residual defects, consisting most often of a mild cognitive impairment., Conclusions: The EEG as an investigation of brain function can be crucial in establishing the organic nature of disease. MRI is important to exclude other diffuse or multifocal encephalopathies. However, in contrast to previous reports in the literature abnormal MRI should not be considered mandatory in adult ADEM. Difficulties in the diagnosis of ADEM are discussed and the importance of clinical and paraclinical findings for establishing the diagnosis is outlined.

An arteriovenous malformation (AVM) consists of one or more arteries that drain through one or several small openings directly into one or more veins. The capillary system between arteries and veins is missing. The natural history of an unruptured AVM demonstrates a 1-2% bleeding rate and once ruptured a 2-4% annual risk of rebleeding. There is a risk of dying of AVM up to 1% per year, a 1% annual risk of developing de novo epilepsy, and a 1% chance of disability per year. Small AVMs are more likely to rupture than large AVMs. The goal of treatment is complete obliteration of the malformation. The risk of surgical treatment depends mainly on its size, location and drainage pattern. Size and angioarchitecture determine the risks of embolotherapy and radiotherapy. AVMs in Spetzler-Martin grades I-III should be treated by microneurosurgery or a combination of embolotherapy and microneurosurgery. They can be excised with low surgical mortality and morbidity. For AVMs in Spetzler-Martin grades IV and V staged treatment approaches such as embolotherapy followed by surgery or radiotherapy should be considered. Rarely is embolotherapy or radiotherapy alone indicated. There are AVMs in Spetzler-Martin grades IV and V that may be inaccessible for surgical or any other treatment, and that should be left alone. Prospective randomised trials on the optimal management of AVMs are lacking. All our knowledge on AVMs stems from open series and indirect comparisons.

We compared three angiographic methods for grading of carotid stenosis and examined the correlation between angiographic and ultrasound findings. Two observers independently measured 111 carotid stenoses on arteriographic films of 84 patients. The stenoses were graded according to the European Carotid Surgery Trial (ECST), North American Symptomatic Carotid Endarterectomy Trial (NASCET), and Common Carotid (CC) methods. The results obtained by these methods were compared, and the interobserver reproducibility of the measurements was calculated. In addition, all angiographic results were compared to ultrasound findings obtained before angiography. Measurements using the CC method were the most reproducible and those using the NASCET method the least. The NASCET method underestimated the degree of stenosis compared to the other methods. The ECST and CC methods yielded almost identical results (97% agreement). Ultrasound provided an accuracy of 94% compared to ECST and CC methods and 84% compared to the NASCET method. Interobserver reproducibility of angiographic quantification of carotid stenoses was best for the CC and ECST methods and least for the NASCET method. Ultrasound demonstrated better accuracy than the ECST and CC methods.

Pulsatile tinnitus can be annoying for a patient and can also be the only clue to a potentially devastating and life-threatening disease. In order to understand its clinical spectrum and management better we analysed the files of 84 patients seen at our institution over a 10-year period. Noninvasive techniques (ultrasound, computed tomography, magnetic resonance imaging) and angiography were employed as investigations tailored to the individual patient. A vascular disorder [i.e. arteriovenous fistula, dissection of the internal carotid artery (ICA), fibromuscular dysplasia, aneurysm of the ICA and sinus thrombosis] was found in 36 patients (42%), most commonly a dural arteriovenous fistula or a carotid-cavernous sinus fistula. In 26 patients with a vascular abnormality, pulsatile tinnitus was the presenting symptom. In 12 patients (14%), nonvascular disorders such as glomus tumour or intracranial hypertension with a variety of causes explained the tinnitus. We conclude that patients with pulsatile tinnitus should be investigated with noninvasive techniques. If these are negative or to clarify abnormal findings of noninvasive techniques selective angiography is needed for diagnosis and to guide treatment.

A transcranial colour-coded duplex sonography (TCCD) study was performed to establish reliable criteria for the assessment of collateral flow through the anterior (ACoA) and posterior (PCoA) communicating artery without using compression tests. We studied 86 patients with angiographically evaluated unilateral > 69% stenosis (n = 53) and occlusion (n = 33) of the carotid artery. The following TCCD criteria were evaluated: for diagnosis of cross-flow through the ACoA, detection of reversed flow in the anterior cerebral artery (ACA) on the obstructed (ipsilateral) side. For the diagnosis of cross-flow through the PCoA: (A) identification of the PCoA; (B) peak systolic velocity in P1 posterior cerebral artery (PCA) higher than the mean value + 2 SD of normals; (C) ratio of ipsilateral peak systolic P1 PCA velocity to peak systolic P1 PCA velocity to peak systolic P2 PCA velocity higher than the mean ratio + 2 SD of normals; (D) ratio of ipsilateral peak systolic P1 PCA velocity to contralateral peak systolic P1 PCA velocity higher than the mean ratio + 2 SD of normals; (E) peak systolic basilar artery velocity higher than the mean value + 2 SD of normals. Eight patients (9%) with inadequate temporal ultrasonic windows were excluded. The sensitivity and specificity for TCCD evaluation of ACoA cross-flow were 100%. Using criteria A and B the corresponding values for the PCoA were 85 and 98%, respectively. Criteria C-E were not useful owing to lower sensitivity. In conclusion, we delineated TCCD criteria that make it possible to assess reliably the cross-flow through the circle of Willis in patients with adequate ultrasonic windows.

From 1980 to 1992 we followed 12 patients with cardiac myxomas for an average of 4.4 years (8 months-11 years). Presenting symptoms were neurological in four patients (hemiparesis, aphasia, visual field deficits, progressive dementia or vertigo), progressive dyspnoea in six, pulmonary embolism in one, and peripheral arterial or renal emboli in three. The diagnosis was suspected clinically in 11 patients. It was confirmed by echocardiography in ten and by thoracic CT in one. All these patients had cardiac surgery. One diagnosis was made at autopsy; the patient died unexpectedly during surgery for emboli to the leg arteries. At follow-up, two additional patients had died, one from myocardial infarction and one from rhabdomyosarcoma. Only one of the nine surviving patients had recurrent symptoms after cardiac surgery. His dementia continued to progress. The patients without new symptoms after cardiac surgery had normal MRI of the brain or residual ischaemic lesions. MRI of the patient with progressive dementia showed multiple cerebral lesions with a bright centre and a dark rim on T1- and T2-weighted spin-echo images. On CT there were many calcified lesions. CT, MR angiography and contrast angiography revealed multiple fusiform aneurysms. The rare occurrence of progressive neurological symptoms after myxoma resection with multiple cerebral lesions and aneurysms should suggest myxoma metastases to the brain.

We present two cases with acute onset of vertical gaze palsy, mainly consisting of impaired downgaze and apraxia of downward head movements, together with neuropsychological deficits (hypersomnia, impaired attention and disorders of memory and affective control). CT and MRI revealed bilateral post-ischaemic lesions in the dorsomedial thalamus and the mesodiencephalic junction, dorsomedial to the red nucleus, thus being restricted to the territory of the posterior thalamosubthalamic paramedian artery, which includes the region of the rostral interstitial nucleus of the medial longitudinal fascicle as the main premotor nucleus for the generation of vertical saccades. In our patients, oculographic examination with electro-oculography and magnetic search coil recording showed severe impairment of downward more than upward saccades and only minor deficits of vertical pursuit and the vestibulo-ocular reflex. Visual functions were normal, with one exception: a psychophysical test of motion perception revealed a significant deficit in the detection of vertical movements. This could be due to a central adaptive mechanism which, in order to minimize oscillopsia, might elevate thresholds for vertical motion perception in cases of vertical gaze palsy. As an alternative explanation, lesions within the midbrain tegmentum could have damaged subcortical visual pathways involved in motion perception.

The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system. The incidence of thiamine deficiency was 31%, of riboflavin deficiency 22% and of pyridoxine deficiency 6%. Alcoholics in particular suffered from deficiencies of vitamin B 1, and B 2. There was a correlation of vitamin B 1 and B 2 deficiency and signs of a cerebellar and/or brainstem lesion. The most frequent symptoms in this connection were gait disturbances and oculomotor signs like spontaneous and gaze nystagmus, disturbed eye tracking, diminished optokinetic nystagmus, decreased ability to suppress vestibular nystagmus by fixation. These signs hardly ever occurred in alcoholic patients who showed no deficiency of vitamin B 1, B 2 or B 6. Whenever they do appear, a vitamin B supplementation has to be performed in order to prevent the manifestation of Wernicke's encephalopathy, cerebral or cerebellar atrophy. Alcoholics showed the same incidence of polyneuropathy, whether they suffered from a deficiency of B vitamins or not. Deficiencies of vitamin B 1, B 2 or B 6 were also found in patients with intestinal malabsorption and polyneuropathy, diabetic polyneuropathy, optic atrophy, myelopathy and cerebellar ataxia of unknown etiology, neurological manifestations of neoplasms arising outside the nervous system, B 12 myeloencephalopathy and Thévenard's syndrome.

The spectrum of clinical signs in cases of superior sagittal sinus thrombosis includes not only focal neurological deficits, seizures and mental disturbances, but also symptoms which may lead to a diagnosis of pseudotumour cerebri (PTC). In 14 cases of angiographically (or autopsy) proven thrombosis of the superior sagittal or both lateral sinuses, the "empty triangle" sign on contrast CT examination was the most reliable sign, suggesting the diagnosis in 70%. Indirect CT signs (venous infarcts) were observed in all 8 patients with focal neurological signs, but appeared rather delayed in 3 cases. In contrast, patients with "benign" intracranial hypertension or PTC (6 cases) had normal unenhanced scans (4 cases) or showed slight diffuse brain oedema (2 cases). Magnetic resonance imaging was performed in 4 patients with findings suggestive of intravascular coagulation; however, due to the complexity of flow phenomena, further studies employing this new imaging technique will first have to be performed. Thus, angiography remains the best diagnostic tool and should not be delayed if there is a clinical suspicion of thrombosis.

There is still a need to prove that even static magnetic fields up to 1.5 T used in magnetic resonance imaging (MRI) are biologically safe and harmless for humans. Recordings of median and ulnar nerves and brain-stem auditory evoked potentials in 20 patients were completed prior to and after MRI investigation of the central nervous system. Neither the somatosensory nor the auditory evoked potentials exhibited any significant change of latencies, interpeak latencies or amplitudes. Since these electrophysiological parameters are highly dependent on the quality of nerve conduction and integrity of information processing in various nuclei, it may be assumed that MRI causes no lasting changes in either respect.

Magnetic resonance imaging (MRI) patterns of 11 haemangioblastomas examined with a 1.5-T scanner are described. MRI was as effective as contrast-enhanced CT in the detection of vascular tumour components, but was less sensitive than angiography. MRI was superior to CT in delineating the exact extent of the lesions, for example contact with the arachnoid surface. Even if a cystic tumour component is absent, MRI can provide helpful criteria for differential diagnosis; in particular, T2 values allow differentiation from meningiomas. In three patients additionally administered gadolinium (Gd) diethylenetriaminepenta-acetic acid (DTPA) the angiomatous parts of the tumour showed a remarkable decrease in T1 value, but the time dependence of the enhancement was not the same as that seen in dynamic CT.

A case of paraneoplastic cerebellar degeneration (PCD) associated with Hodgkin's disease is presented. The features that make this case particularly interesting are the simultaneous occurrence of PCD with a relapse of Hodgkin's disease, which has been present for 17 years, and the arrested progression of cerebellar dysfunction after a subacute onset. Cerebellar atrophy was revealed by computed tomography and magnetic resonance imaging. In contrast to two previously reported cases, anti-Purkinje-cell antibodies were not detected.