Tiemo Wessels

Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes

Background— A number of clinical syndromes describing the presentation of deep brain infarcts are called lacunar syndromes resulting from small vessel occlusion (SVO). To verify the reliability of the clinical diagnosis “lacunar syndrome,” the value was investigated with diffusion-weighted MRI (DWI). Methods and Results— A total of 73 patients (mean age 66 years; range 35 to 83 years) with sudden onset of a classical lacunar syndrome were enrolled. On the basis of the DWI findings, patients were divided into 3 groups: group 1, single subcortical lesion (<15-mm lesion; 43 patients; 59%); group 2, large (≥15 mm) or scattered lesions in 1 vascular territory (16 patients; 22%); and group 3, multiple lesions in multiple vascular territories (14 patients; 19%). A stroke mechanism other than SVO could be identified in 17 (23%) patients. Cardiac work-up revealed a cardiac embolic source in 8 patients (11%). Duplex sonography revealed symptomatic stenosis in 9 patients (12%). Based on the work-up information, 29 patients (40%) were found to have a potential cause of stroke other than SVO. A significant correlation with >1 single lesion on DWI-MRI and a clinical proven embolic source was observed (P=0.002). In 9 patients with MRI suspicious for a pathomechanism other than SVO, no embolic source was found. Conclusions— The use of DWI-MRI improves the accuracy of the subtype diagnosis of stroke. Inaccuracy has to be expected in approximately one third if lacunar diagnosis is based on clinical and computed tomography findings. Most of these “false-positive” cases are attributable to large artery or cardiogenic embolic stroke.

Embolic Lesion Pattern in Stroke Patients With Patent Foramen Ovale Compared With Patients Lacking an Embolic Source

Background and Purpose— Multiple acute ischemic lesions on diffusion-weighted magnetic resonance imaging (DWI-MRI) are thought to be of embolic origin. However, in several patients with multiple ischemic lesions on DWI-MRI, no embolic source was detected, despite a thorough clinical work-up. Stroke etiology in such cases is then classified as cryptogenic. In other patients, a potential embolic source is limited to a patent foramen ovale (PFO) that may act as an embolic source of unsure relevance. We therefore examined the prevalence of the multiple-lesion pattern in patients with cryptogenic stroke compared with patients with PFO. Methods— We screened 650 stroke patients by DWI-MRI. For the subsequent evaluation, we excluded patients with a cardiac embolic source other than PFO, symptomatic carotid artery disease, and other apparent stroke causes, such as dissection or vasculitis, and patients whose diagnostic work-up was incomplete. For the remaining 106 patients, we found DWI lesions in 73, who were subjected to further evaluation. Results— There were no differences in the occurrence of the multiple-lesion pattern in patients with cryptogenic stroke compared with patients with PFO, either for the entire group or for the subgroup of young stroke patients who were <50 years old. Patients with PFO showed a significantly higher incidence of multiple lesions in the posterior circulation. Conclusions— The multiple-lesion pattern on DWI-MRI is not uncommon, even when extensive testing does not reveal any embolic source. Therefore, it is not possible to discriminate between cryptogenic stroke and stroke from an assumed paradoxical embolism.

A new model of reversible sinus sagittalis superior thrombosis in the rat: magnetic resonance imaging changes.

OBJECTIVE: The causes of cerebral sinus and vein occlusion and the accompanying parenchymal changes remain largely unexplained. The clinical variability and low incidence of the disease complicate systematic clinical investigations. Animal studies are indispensable; however, existing animal models of sinus thrombosis do not allow for long-term follow-up studies and are not suitable for pharmacological recanalization because sinus thrombosis is induced by ligation and injection of thrombogenic substances and does not resemble sinus thrombosis in humans. METHODS: We induced thrombosis of the superior sagittal sinus (SSS) by careful topical application of ferric chloride onto the SSS of rats, leading to highly reproducible occlusions. Magnetic resonance imaging was performed immediately after initiation of thrombosis and on postoperative Days 1, 2, and 7. Diffusion- and T2-weighted images allowed for calculation of the apparent diffusion coefficient and T2 relaxation time. Vascular status was assessed by venous magnetic resonance angiography. Neurological deficits were assessed with the rotarod test. RESULTS: Seven days after induction of thrombosis, partial recanalization (50.7% of the SSS remaining occluded) was accompanied by a resolution of early generalized changes of the apparent diffusion coefficient and of T2 relaxation time, indicating edema of the entire brain parenchyma. Compared with sham-treated animals, clinical skills in the experimental group improved over time, which was statistically independent from the degree of recanalization. Histopathological analysis revealed no signs of cerebral infarction. CONCLUSION: This is the first animal model of SSS thrombosis that offers the possibility to investigate pathophysiological aspects of the disease as well as the influence of therapy on the nature of disease progression.

Upper cranial nerve palsy resulting from spontaneous carotid dissection

AbstractIntroductionUpper cranial nerve palsy has a variety of causes such as cerebral and nerve ischemia, diabetes, infectious and non–infectious meningitis, subarachnoid hemorrhage and intracranial aneurysm.Case 1A 45–year–old man suffered from holocephalic headaches and a rightsided neck pain for two weeks. He presented to our emergency department because of a sudden ptosis of the right eye. On admission neurological examination revealed a right sided Horner’s syndrome and hypesthesia of the right side of the face. Magnetic resonance angiography identified a circumscribed dissection of the right extracranial internal carotid artery originating from the carotid bifurcation. Conventional angiography 2 weeks later showed a nearly recanalized artery.Case 2A 55–year–old previously healthy man without cardiovascular risk factors developed right sided neck pain when loading a seeder with several sacks of crop. A few hours later he noticed a left–sided weakness. On admission a severe left sided hemiparesis and a mild neglect were present. Duplex sonography revealed a right–sided distal internal carotid artery (ICA) occlusion. The next morning the patient complained of double vision; he had a right–sided pupil–sparing oculomotor palsy. The diagnosis of ICA dissection was confirmed by conventional angiography, at that time showing a partially recanalized ICA without involvement of the cavernous region by the dissection.ConclusionICA dissection must be included in the differential diagnosis of upper cranial nerve palsy and should be assessed by duplex ultrasound and magnetic resonance imaging. A possible explanation is nerve ischemia due to a transient or permanent interruption of the blood supply by compression of the vasa nervorum originating from the intracranial carotid artery.

Isolierte Hirnnervenausfälle bei Karotisdissektionen

ZusammenfassungEin isolierter Hirnnervenausfall kann eine Vielzahl verschiedener Ursachen haben wie z.B.eine Hirnstammischämie, eine Ischämie der Vasa nervorum bei Diabetes mellitus, Subarachnoidalblutungen, infektiöse und nichtinfektiöse Meningitiden, Metastasen im Bereich der Schädelbasis, des Hales oder des oberen Mediastinums, enzündliche Erkrankungen wie beispielsweise eine Sarkoidose oder ein Tolosa-Hunt-Syndrom,Prozesse im Sinus cavernosus und Aortenaneurysmen. Die Karotisdissektion ist eine seltene Ätiologie eines isolierten Hirnnervenausfalls-wir stellen hierzu zwei Fallbeispiele vor und geben einen Überblick über die aktuelle Literatur. Eine fehlende Behandlung hat möglicherweise fatale Folgen für den Patienten. Daher sollte die Karotisdissektion in die differenzialdiagnostischenÜberlegungen miteinbezogen werden.Der Nachweis sollte mittels Farbduplexsonographie und/oder MR-Tomographie erfolgen.SummaryCranial nerve palsy has a variety of causes such as cerebral ischemia, nerve ischemia in diabetes, infectious and noninfectious meningitis, subarachnoid hemorrhage, malignant tumors of the skull base, neck, or upper mediastinum, aortic aneurysm, surgery of the thyroid,and many more.We report two cases of spontaneous carotid dissections leading to cranial nerve palsies, which is an uncommon cause of isolated cranial nerve palsies.ICA dissection must therefore be included in the differential diagnosis of lower cranial nerve palsy and should be assessed by duplex ultrasound and MRI as is demonstrated in our cases.