Perfusion-weighted MRI to evaluate cerebral autoregulation in aneurysmal subarachnoid haemorrhage.

INTRODUCTION: The aim of this study was to evaluate autoregulatory mechanisms in different vascular territories within the first week after aneurysmal subarachnoid haemorrhage (SAH) by perfusion-weighted magnetic resonance imaging (PW-MRI). For this purpose, regional cerebral blood flow and volume (rCVF and rCBV) were measured in relation to different degrees of angiographically visible cerebral vasospasm (CVS). MATERIALS AND METHODS: In 51 SAH patients, PW-MRI and digital subtraction angiography were performed about 5 days after onset of SAH. Regional CBF and rCBV were analysed in the territories of the anterior cerebral artery (ACA), the middle cerebral artery (MCA) and the basal ganglia of each hemisphere in relationship to the degree of CVS in the particular territory. Correlations between rCBF, rCBV and CVS were analysed. RESULTS: CVS was found in 22 out of 51 patients in at least one territory. In all territories, rCBV decreased with increasing degree of CVS, correlated with a decrease of rCBF. In the ACA territories, SAH patients with severe CVS had significantly lower rCBF compared to healthy subjects and to SAH patients without CVS. In the basal ganglia, rCBF and rCBV of the control group were significantly higher compared to the patients without and with moderate vasospasms. CONCLUSION: PW-MRI showed simultaneous decrease of rCBF and rCBV in patients with SAH. The fact that rCBV did not increase in territories with CVS to maintain rCBF reveals dysfunctional vascular autoregulation. Vasospasms in the microvasculature are most evident in the basal ganglia, showing decreased rCBV and rCBF even in SAH patients without CVS.

A novel dynamic model for experimental spinal cord compression.

OBJECT: The goal of this study was to develop a novel dynamic model for experimental spinal cord compression that closely approximates neoplastic epidural compression of the spinal cord in humans. METHODS: In 30 New Zealand white rabbits, the thoracic spine was exposed via a posterior approach. On each side of one vertebral lamina a small hole was drilled caudal to the articular process. A silicone band was passed through these holes, forming a loop. The spinal dura mater was exposed via an interlaminar approach. The loop was brought into contact with the dura mater and fixed in its position encircling 270 degrees of the circumference of the spinal cord. Thereafter, the loop was gradually tightened at set times by pulling at the ends of the band and fixing them again in their new position. The spinal cord was thus increasingly compressed in a circular and dynamic manner. Neurological deficits of various degrees were created in all animals in the compression group, and the compressive effect of the loop was reliably demonstrated on MR imaging. After decompression of the spinal cord, the neurological deficits were reversible in the majority of animals, and MR imaging revealed either no signal changes or only circumscribed ones within the cord. In contrast, MR images obtained in animals that did not recover revealed the occurrence of extensive chronic myelopathy. CONCLUSIONS: This novel model features reproducibility of paresis and neurological recovery. It is a dynamic model simulating circular tumor growth and is characterized by its easy, straightforward, and cost-saving applicability.

Assessment of vasospasm in experimental subarachnoid hemorrhage in rats by selective biplane digital subtraction angiography.

Although the rat subarachnoid hemorrhage model is well established in vasospasm research, the angiographic evaluation is difficult due to the animal's small size. For this reason, the aim of the study was to develop a standardized angiographic examination technique without additional complex equipment. Under general anesthesia, 11 Sprague-Dawley rats underwent selective cerebral digital subtraction angiography using a 0.3 mm focal spot and a 2.0-fold linear magnification. Five animals had experimental subarachnoid hemorrhage according to the "double-hemorrhage" model. Comparison with the intraarterial tip of the microcatheter enabled calibration of the vessel lumen. The diameter of the normal basilar artery (n=6) was 0.34+/-0.03 mm (mean+/-SD), whereas delayed vasospastic constriction (mean 6.2 days) caused a reduction in diameter of 32.4% (0.23+/-0.09 mm) as well as impaired collateral blood flow via the posterior communicating artery and anterior spinal artery. Histological examination of sections stained with hematoxylin and eosin under a light microscope confirmed vasospasm. In conclusion, biplane digital subtraction angiography allows precise and reliable evaluation of arterial diameter reduction and hemodynamic parameters in a rat vasospasm model. However, further investigation is required for assessment of vasoactive drugs, e.g., endothelin receptor antagonists.

Time course in the development of cerebral vasospasm after experimental subarachnoid hemorrhage: clinical and neuroradiological assessment of the rat double hemorrhage model.

OBJECTIVE: The "double hemorrhage" model in the rat is frequently used to simulate delayed cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in humans. However, an exact neurological and angiographic characterization of the CVS is not available for this model so far and is provided in the present investigation. Additionally, perfusion weighted imaging (PWI) at 3 tesla magnetic resonance (MR) tomography was implemented to assess the reduction in cerebral blood flow (CBF). METHODS: In a prospective, randomized setting CVS was induced by injection of 0.2 ml autologous blood twice in the cisterna magna of 45 male Sprague-Dawley rats. The surviving animals were examined on Days 2, 3, 5, 7 and 9 and compared to a sham operated control group (n = 9). Rats were neurologically graded between 0 and 3, followed by MRI and selective digital subtraction angiography (DSA). The relative CBF was set in relation to the perfusion of the masseter muscle. RESULTS: The neurological state was significantly worsened on Day 2 (Grade 3), 3 (Grade 3), and 5 (Grade 2) (medians). The relative CBF/muscle BF ratio (2.5 +/- 0.8 (SAH) versus 9.2 +/- 1.3 (sham) (mean +/- SEM) and the basilar artery (BA) diameter (0.15 +/- 0.02 mm (SAH) versus 0.32 +/- 0.01 mm (sham) were significantly decreased on Day 5. Correlation between relative CBF/muscle BF ratio and BA diameter was 0.70. CONCLUSION: A valid and reproducible CVS simulation was proven by neurological score, DSA, and PWI on Day 5. Furthermore, our data demonstrate the practicability and validity of MR PWI for the monitoring of CVS in a rat SAH model.

Cerebral Erdheim-Chester disease: case report and review of the literature.

Erdheim-Chester disease is a rare systemic non-Langerhans histiocytosis of unknown etiology that affects multiple organ systems. Cerebral involvement is most often caused by extra-axial masses of foamy histiocytes, whereas intraparenchymal manifestations are less frequent. Review of the literature yielded a total of seven patients with increased signal intensities on T2-weighted images in both dentate nuclei and the peridentate regions. We report on a 44-year-old man with biopsy-proven Erdheim-Chester disease and slowly progressive cerebellar dysfunction. MRI showed additional symmetrical hyperintense signal changes in the superior cerebellar peduncle as well as in the trigonum lemnisci on coronal FLAIR images. The widespread neurological manifestations of cerebral Erdheim-Chester disease and differential diagnosis are discussed.