Stefan Weidauer

Impairment of Cerebral Perfusion and Infarct Patterns Attributable to Vasospasm After Aneurysmal Subarachnoid Hemorrhage A Prospective MRI and DSA Study

Background and Purpose— The objective of this study was to investigate disturbance of perfusion and infarct patterns attributable to cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). Methods— One hundred seventeen patients with aneurysmal SAH specifically selected at high risk for CVS were enrolled in this prospective study. One hundred twelve patients underwent surgical (n=63) or endovascular (n=59) therapy. For assessment of CVS, relative diameter changes of proximal and distal vessel segments on follow-up angiography at day 7±3 after SAH were analyzed in relation to baseline measurements, and cerebral circulation times were measured. Postprocedure MRI was undertaken selectively at four time points: within 3 days, between days 4 and 6, day 7 to 14, and day 15 to 28 from onset of SAH, including perfusion- and diffusion-weighted images. Procedure-related lesions were excluded and CVS-associated infarct patterns analyzed. Results— Occurrence of angiographic CVS was as high as 87.5% between days 7 and 14 and 52.5% showed new infarcts. Eighty-one percent of the infarcts were related to severe CVS (vascular narrowing >66%) and significant (P<0.001) cerebral circulation times prolongation of 8.47±2.25 seconds (time-to-peak delay on perfusion-weighted image: 6.52±4.75 seconds), 16% were associated with moderate CVS (34% to 66% vascular narrowing; cerebral circulation times prolongation: 4.72±0.66 seconds). Besides territorial (47%), lacunar (20%), and watershed infarcts (26%), in 7%, band-like cortical lesions developed without evidence for severe CVS. Conclusions— CVS after SAH may involve the complete arterial system from the circle of Willis up to the distal vessel segments. Depending on the variable types of collateral flow, location of affected vessels segments as well as the degree of CVS may induce different infarct patterns.

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.

Intraoperative motor evoked potential alteration in intracranial tumor surgery and its relation to signal alteration in postoperative magnetic resonance imaging.

OBJECTIVETo determine the degree to which the pattern of intraoperative isolated, unilateral alteration of motor evoked potential (MEP) in intracranial surgery was related to motor outcome and location of new postoperative signal alterations on magnetic resonance imaging (MRI). METHODSIn 29 patients (age, 42.8 ± 18.2 years; 15 female patients; 25 supratentorial, 4 infratentorial procedures), intraoperative MEP alterations in isolation (without significant alteration in other evoked potential modalities) were classified as deterioration (> 50% amplitude decrease and/or motor threshold increase) or loss, respectively, or reversible and irreversible. Postoperative MRI was described for the location and type of new signal alteration. RESULTSNew motor deficit was present in all 5 patients with irreversible MEP loss, in 7 of 10 patients with irreversible MEP deterioration, in 1 of 6 patients with reversible MEP loss, and in 0 of 8 patients with reversible MEP deterioration. Irreversible compared with reversible MEP alteration was significantly more often correlated with postoperative motor deficit (P < .0001). In 20 patients, 22 new signal alterations affected 29 various locations (precentral gyrus, n = 5; corticospinal tract, n = 19). Irreversible MEP alteration was more often associated with postoperative new signal alteration in MRI compared with reversible MEP alteration (P = .02). MEP loss was significantly more often associated with subcortically located new signal alteration (P = .006). MEP deterioration was significantly more often followed by new signal alterations located in the precentral gyrus (P = .04). CONCLUSIONMEP loss bears a higher risk than MEP deterioration for postoperative motor deficit resulting from subcortical postoperative MR changes in the corticospinal tract. In contrast, MEP deterioration points to motor cortex lesion. Thus, even MEP deterioration should be considered a warning sign if surgery close to the motor cortex is performed.

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.

Posterior encephalopathy with vasospasm: MRI and angiography

Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously.

Diffusionsgewichtete MRT bei spinalen Infarkten

ZusammenfassungSpinale Infarkte sind selten und haben eine heterogene Ätiologie. Die in der Akutdiagnostik eingesetzte spinale Magnetresonanztomographie (MRT) dient vor allem dem differenzialdiagnostischem Ausschluss spinaler Raumforderungen, die einer raschen neurochirurgischen Entlastung bedürfen. Wir berichten über 2 Patienten mit einem Syndrom der A. radicularis magna (Adamkiewicz) und Infarzierung des thorakolumbalen Myelons einschließlich des Conus medullaris. Während die T2-gewichteten Sequenzen 4 und 28 h nach dem Infarktereignis keine beziehungsweise nur diskrete unspezifische Signalanhebungen zeigten, ergab die ergänzende diffusionsgewichtete Bildgebung (DWI) eine deutliche Diffusionsstörung. Vergleichbar mit der modernen MRT-Diagnostik bei akuten zerebralen Infarkten hebt die Diskrepanz zwischen minimalen Signalveränderungen in den T2-gewichteten Sequenzen und deutlicher Diffusionsstörung den Stellenwert der DWI in der Akutdiagnostik spinaler Infarkte hervor. Allerdings stehen systematische DWI-Untersuchungen bei akuten entzündlichen und vaskulären spinalen Prozessen noch aus.SummarySpinal cord infarctions occur rarely and are due to various aetiologies. In an emergency setting with acute spinal cord symptoms, magnetic resonance imaging (MRI) is used to exclude space-occupying lesions which require neurosurgical intervention. We report on two patients presenting with an anterior spinal artery syndrome caused by infarction of the thoracolumbar spinal cord including the conus medullaris. While T2-weighted images 4 h and 28 h after onset of clinical symptoms showed only slight unspecific signal changes, diffusion-weighted imaging revealed clear infarction and detected spinal cord ischaemia in an early stage, showing signal intensity conversion comparable to that in acute cerebral stroke.

Effect of delayed cerebral vasospasm on cerebrovascular endothelin A receptor expression and function

OBJECT The key role in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH) is increasingly assigned to endothelin (ET)-1. Constriction of the cerebrovasculature by ET-1 is mainly mediated by the ET(A) receptor but is putatively altered during the development of cerebral vasospasm. Therefore, the aim in the present study was to characterize these alterations, with the emphasis on the ET(A) receptor. METHODS Cerebral vasospasm was induced using the rat double-hemorrhage model and proven by perfusion weighted magnetic resonance imaging. Rats were killed on Day 5 after SAH, and immunohistochemical staining for ET(A), receptors was performed. The isometric force of basilar artery ring segments with (E+, control group) and without (E-, SAH group) endothelial function was measured. Concentration effect curves (CECs) for ET-1 were constructed by cumulative application in the absence and presence of the selective ET(A) receptor antagonist clazosentan (10(-8) or 10(-7) M). RESULTS The CEC for E+ segments was significantly shifted to the left after SAH by a factor of 3.7, whereas maximum contraction was unchanged. In E- segments, the CECs were not shifted during cerebral vasospasm but the maximum contraction was significantly enhanced. The inhibitory potency of clazosentan yielded a pA2 value of 8.6 +/- 0.2. Immunohistochemical staining of the smooth-muscle layer showed no significant increase of ET(A) receptor expression, but positive staining occurred in the endothelial space after SAH. CONCLUSIONS The present data indicate an enhanced contractile effect of the smooth-muscle ET(A) receptors in cases of cerebral vasospasm. The inhibitory potency of clazosentan on this contraction is increased. Furthermore, some evidence for an ET(A) receptor and an endothelium-dependent vasoactive effect after SAH is provided.

Perfusion–diffusion mismatch in MRI to indicate endovascular treatment of cerebral vasospasm after subarachnoid haemorrhage

Introduction Endovascular treatments such as transluminal balloon angioplasty and intra-arterial nimodipine represent rescue therapy for cerebral vasospasm (CVS) after aneurysmal subarachnoid haemorrhage (SAH). Both indication and data regarding its efficacy in the prevention of cerebral infarct are, however, inconsistent. Therefore, an MR based perfusion weighted imaging/diffusion weighted imaging (PWI/DWI) mismatch was used to indicate this treatment and to characterise its effectiveness. Methods MRI was performed for suspicion of CVS. For quantitative evaluation, the brain was partitioned into 19 arbitrary segments of comparable volume. Segments with PWI/DWI mismatch were defined as ‘segment at risk (SR)’. In these cases, MRI was followed by angiography (digital subtraction angiography (DSA)) including endovascular treatment. 48±12 h after treatment, a second MRI was performed and the treatment was repeated if new or remaining SR were observed. Efficacy was classified as the percentage of reduced diameter of the proximal cerebral arteries on DSA following the treatment: mild (≥33%), moderate (34–66%) or severe (≥67%). Results 48 treatment cycles, each consisting of MRI, DSA and a second MRI, were performed in 25 patients. During these cycles, 95 SR were identified. The infarct rate was significantly higher in SR (37%) compared with segments without risk (4%). The infarct rate in SR was significantly reduced if mild proximal CVS could be achieved. In the case of persistent severe CVS, infarcts occurred in all SR. Conclusion The present series suggests that PWI/DWI mismatch is predictive of the development of infarct in the case of CVS. The infarct rate could, however, be improved if proximal CVS was sufficiently reduced.

Diffusion tensor tracking of fornix infarction

Focal damage to the fornices is uncommon and may be due to surgical removal of ventricular cysts and tumours.1 We report a case of bilateral fornix infarction with reduced fractional anisotropy values at 3 T after anterior communicating artery aneurysm clipping. A healthy 33-year-old woman was admitted to our hospital with the incidental finding of an anterior communicating artery (ACoA) aneurysm on magnetic resonance angiography. Neurological examination was normal. Digital subtraction angiography visualised a broad based, tapered and 4 mm sized aneurysm of the ACoA and a median callosal artery (fig 1C). The ACoA aneurysm was treated with surgical clipping because of its irregular configuration. After surgery, the patient was drowsy with fluctuating impaired vigilance. She was disoriented in time, space and person, and revealed anterograde amnesia and amnesic aphasia. Her relatives noticed personality changes, psychomotor slowing and decreased spontaneity of speech and behaviour. Apart from transient mild right sided facial paresis, motor function of the limbs, deep tendon reflexes, sensory and coordinative examination and cranial nerves were normal. During the next 5 weeks of neurological rehabilitation, cognitive performance improved considerably. Seven weeks after the operation, she was orientated in all qualities and initial deficits in attentional performance and executive functions recovered. However, neuropsychological testing at this time revealed an average performance on …

Comparison of intracranial 3D‐ToF‐MRA with and without parallel acquisition techniques at 1.5t and 3.0t: preliminary results

Purpose: To evaluate the performance of four 3D‐ToF magnetic resonance angiography (MRA) sequences with and without integrated parallel acquisition techniques (iPAT) at 1.5T and 3.0T in imaging intracranial vessels. Material and Methods: Seven volunteers and 5 patients (4 aneurysms, 1 AVM) underwent 3D‐ToF‐MRA at 1.5T (Magnetom Sonata) and 3.0T (Magnetom Trio) with and without parallel acquisition techniques (iPAT) using similarly designed 8‐channel phased‐array head coils. Imaging time of the pulse sequences was set to 7.15 and 7.35 min, respectively. Images were analyzed quantitatively by calculating signal‐to‐noise (SNR) and contrast‐to‐noise (CNR) ratios of proximal M2 segments and qualitatively by using a 5‐point scale. Results: SNR and CNR were significantly higher for both 3D‐ToF sequences at 3.0T compared with both pulse sequences at 1.5T. The highest SNR and CNR were obtained at 3.0T without iPAT. However, because of a higher spatial resolution (matrix 512×640) visualization of small vessel details was best at 3.0T with iPAT. Conclusion: Intracranial 3D‐ToF‐MRA at 3.0T offers superior image quality compared with 1.5T, particular in the delineation of smaller vessels. In contrast to 1.5T, implementation of iPAT at 3.0T is of additional benefit since the high SNR available at 3.0T allows for higher spatial resolution without prolongation of measurement time.