Malignant "Angioglioma": Clinical, Radiologic, and Histopathologic Features.

BACKGROUND: Glioblastoma multiforme (GBM) is the most frequent malignant neoplasm in the adult brain. In contrast, arteriovenous malformations (AVMs) are presumably congenital lesions, usually presenting with hemorrhage. Hypervascular low-grade gliomas associated with AVMs were previously called "angioglioma." An association of AVMs and GBM was also described. STUDY AIMS: We discuss the data of the largest series of locally coincident GBM with AVM in a single institution so far. All analyses were explorative only. PATIENTS: We report a series of four patients presenting at our department from 2006 to 2014. All patients underwent surgery. The cases were analyzed regarding initial presentation, clinical findings, tumor localization, and histopathologic results. CONCLUSIONS: A local coincidence of cerebral AVM and GBM is rare. Only a few reports can be found in the literature. The radiologic as well as the clinical presentations are individual. Proangiogenic factors are discussed as involved in the appearance of both entities in the same location. However, the presence of pathologic vessels within malignant gliomas is well known to all neurosurgeons and proangiogenic activity has been proven. Therefore, it seems possible that tumor activity itself contributes to the pathogenesis of a vascular malformation.

Impact of landmark endovascular stroke trials on logistical performance measures: a before-and-after evaluation of real-world data from a regional stroke system of care.

BACKGROUND AND PURPOSE: Endovascular treatment of large-vessel occlusion stroke often necessitates patient transfer by a twin-track approach: endovascular thrombectomy (ET) in endovascular-capable facilities preceded by intravenous thrombolysis in primary stroke centers. We tested the open hypothesis that recent landmark trials on ET had any significant effect on logistical performance measures among different modes of admission. METHODS: We retrospectively categorized 250 patients who presented at our institution as: (A) primarily admitted or transferred from (B) inner-city and (C) regional hospitals. The period from May 2015 to June 2017 was compared with the preceding period of August 2009 to April 2015 with respect to real-life transfer distances and sectional time metrics from symptom onset to angiographic recanalization. RESULTS: Onset-to-recanalization time decreased in the primary admission path, whereas delays persisted for inter-hospital transfer: (A: 261 min (210-315) vs 198 (167-264) P<0.0001; B: 257 (214-306) vs 265 (199- 360) P=0.566; and C: 371 (322-415) vs 346 (307-405) P=0.559). Onset-to-recanalization time was negatively correlated with recanalization success (mTICI; r=-0.4195 P<0.0001). The rate of secondarily referred patients (26% vs 48% P=0.0004) and off-hour presentation (36% vs 44% P=0.004) increased, as did the catchment area (C: 52.2 km (30,4-64,5) vs 64.4 (43,2-78,9) P=0.032). Improvement in door-in-door-out time at the referring hospitals (C: 113 min (30) vs 86 (29) P=0.0236) did not translate into reduced total referral times or the accelerated initiation of ET. CONCLUSION: Recent landmark trials already led to a considerable streamlining of ET workflow if patients were directly admitted. Prehospital time management and triage seem to be the major determinants of optimization.

The Neuroform Atlas stent to assist coil embolization of intracranial aneurysms: a multicentre experience.

OBJECTIVE: To assess the clinical safety and efficacy of the Atlas microstent in stent-assisted coil embolization of wide-necked intracranial aneurysms. METHODS: Single-center observational study in 36 patients (24 female, 12 male, mean age 56 years) with 37 aneurysms for the endovascular treatment of wide-necked aneurysms. After giving informed consent, patients were included according to the following criteria: aneurysm dome-to-neck ratio <2 or neck diameter >4 mm, and a parent vessel diameter of ≤4.5 mm. Primary endpoint for clinical safety was absence of death, absence of major or minor stroke, and absence of transient ischemic attack. Primary endpoint for treatment efficacy was complete angiographic occlusion according to the Raymond-Roy occlusion classification (RROC) immediately after the procedure. RESULTS: In 36/37 (97%) cases, the primary endpoint of safety was reached, one patient had a transitory ischemic attack which completely resolved until discharge. In 31/37 (84%) cases, complete occlusion (RROC 1) was reached, and in 6/36 (17%), a residual neck remained (RROC 2). A sequential approach (first stent, then coiling through the same catheter) was used in 21 cases; the other 16 were treated with the jailing technique. Deployment was technically successful in all cases. Follow-up at a median of 6.1 months was available for 29/37 (78%) aneurysms and showed complete occlusion in 27/29 aneurysms (93%) and a neck remnant in 2 cases (7%). CONCLUSION: Deployment of the Neuroform Atlas microstent is a safe and effective method for the treatment of intracranial wide-necked aneurysms.

Transcranial magnetic stimulation and PAS-induced cortical neuroplasticity in the awake rhesus monkey.

OBJECTIVE: Externally induced neuroplasticity may be of therapeutic value in several neuro-psychiatric disorders. To facilitate research on mechanisms and to make possible the design of prospective, advanced stimulation protocols without exposing human subjects to risk, we have developed a primate model which allows us to assess changes of motor cortical excitability using transcranial magnetic stimulation (TMS). METHODS: TMS hand muscle representation and cortical excitability were determined in two awake trained rhesus monkeys. Neuroplastic changes of cortical excitability were established by 13min of paired associative stimulation (PAS) with interstimulus intervals of either 15 or 5ms. RESULTS: The representational areas of FDI and APB muscles (3.02-4.96cm(2)) were located between the spur of the arcuate and the superior precentral sulcus, indicating the potential to carry out spatially selective cortical stimulation. PAS with an interstimulus interval of 15ms strongly increased cortical excitability for up to two hours, while 5ms interval had no effect. CONCLUSIONS: This first systematic TMS and PAS primate study demonstrates that the trained rhesus monkeys represent an exceptional animal model that allows cortical TMS mapping as well as non-invasive assessment and induction of cortical neuroplasticity. SIGNIFICANCE: This animal model offers additional advantageous options not possible with humans, namely an alternative to invasive, morphological or molecular analyses, making it highly suitable for preclinical development of advanced neuroplasticity paradigms without exposing human subjects to risk.

Iron-deficiency sensitizes mice to acute pain stimuli and formalin-induced nociception.

Iron deficiency has been described as a risk factor in secondary restless legs syndrome (RLS), although it has not been investigated whether iron deficiency induces sensory symptoms in RLS patients. In this study, we established a mouse model of iron deficiency by administering a purified iron-deficient (ID) diet (<8 mg/kg iron) or nonpurified standard diet [normal diet (ND)] (<179 mg/kg iron) to male C57Bl/6 mice from postnatal d 28 for 1, 4, or 15 wk. The level of iron deficiency was assessed by the plasma iron concentration. After varying durations of iron deficiency, both acute and chronic sensory components of pain were measured using hot-plate and formalin tests, which preferentially assess Adelta- and C-fibers, respectively. Based on hot-plate reaction time, ID mice had a lower acute pain threshold than the ND mice after 4 and 15 wk but not after 1 wk. In addition, ID mice had an increased chronic pain response compared with the ND mice only in the late phase of the formalin-test after 1, 4, and 15 wk of iron deficiency. This increased pain response was accompanied by an elevated expression of c-Fos immunoreactive cells at the ipsilateral dorsal horn, suggesting that iron deficiency indirectly increases cell activity at the spinal cord level. These results demonstrate that iron deficiency increases acute and chronic pain responses in mice and may cause similar alterations to the acute pain threshold and sensitivity to C-fiber-mediated chronic pain in ID RLS patients.