Topography of cerebral infarction associated with carotid artery dissection

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%,P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Dopppler sonography.Presented in part at the 3rd European Stroke Conference, Stockholm, May 1994     

137. Fortschritte in der Behandlung extrakranieller Carotisläsionen an der Schädelbasis

Zusammenfassung 25 Patienten mit transitorischen Attacken (9), Insult (15) und lokalen Symptomen (5) wiesen in 4 Fällen bilateral und in 21 Fällen unilateral eine Stenose (20) oder ein Aneurysma (9) der Arteria carotis interna (ACI) an der Schädelbasis auf. Je nach Ätiologie kamen verschiedene Methoden zur Anwendung (Veneninterponat 19, Dilatation 4, Desobliteration 4, tangentialer Clip 1, extraintrakranieller Bypass 1). Die ACI wurde in 19 Fällen bis an die Schädelbasis freigelegt, in 2 Fällen erfolgte mit spezieller Technik die Transplantatanastomose im Carotiskanal (Ischämiezeit 62 min). Die hohe Durchgängigkeitsrate (28/29), das geringe neurologische Defizit (1/29) und die bisherige Rückbildung der Halsnervenausfälle (21/29) zeigen entgegen den Angaben in der Literatur, daß auch in diesem Carotisabschnitt der Rekonstruktion der Vorrang vor allen anderen indirekten Maßnahmen einzuräumen ist.     

Regional cerebral glucose consumption measured by positron emission tomography in patients with Wilson's disease

Using positron emission tomography (PET), the regional cerebral metabolic rate of glucose consumption (rCMRGlc) was measured in 14 patients with Wilson's disease (WD) and 23 normal subjects. In WD patients, cerebellar, striatal and — to a lesser extent — cortical and thalamic rCMRGIc were significantly decreased compared with controls. Striatal rCMRGIc was significantly reduced in those 4 patients who had recently started decoppering therapy as compared with striatal rCMRGlc measured in those 10 patients with longer duration of medication. Caudate rCMRGlc correlated significantly with various signs of extrapyramidal dysfunction. Cerebellar, thalamic and cortical rCMRGlc correlated significantly with the severity of pyramidal signs. These data indicate that the PET measurement of rCMRGIc may be a useful tool to evaluate cerebral involvement in WD and to monitor the response to treatment. Offprint requests to: T. Kuwert     

Tropical pyomyositis

A 22 year old male presented with symptoms of diffuse muscle pain and multiple abnormal laboratory findings that were eventually attributed to tropical myositis. Computed tomography scan was more reliable than ultrasound and served as a guide to needle aspiration and pathologic diagnosis.     

Progress in carotid artery surgery at the base of the skull

From 1977 to 1984, 752 reconstructions of the supra-aortic arteries were performed at our service. In a group of 31 patients presenting with transient ischemic attacks (13) or minor strokes (15), preoperative multiplane angiograms identified lesions from various causes in extremely high locations (fibromuscular dysplasia, 10; atherosclerosis, 6; traumatic changes, 10; spontaneous dissection, 3; and mycotic aneurysms and others, 4) in 34 internal carotid arteries (aneurysms, 10; and stenosis, 24). Surgery was performed on 30 patients. Flow restoration was achieved by resection and vein graft replacement (20), gradual dilatation (5), thromboendarterectomy (6), and tangential clip for exclusion of a lateral aneurysm (1). Only one patient was treated with an extracranial-intracranial anastomosis because the stenosis extended into the carotid siphon. One patient was treated with heparin. Exposure of the internal carotid artery (ICA) at the base of the skull required dissection of the digastric muscle, careful mobilization of the cranial nerves, and detachment of the styloid process in 29 patients. Partial resection of the mastoid process was helpful in two patients. The carotid bone canal was opened from the lateral side in four cases to allow the most distal anastomosis 1 cm within the carotid canal. Back-bleeding was controlled by a balloon catheter. A shunt was impossible to use and clamping time averaged 62 ± 40 minutes. Except for one recurrent stroke and two transient ischemic attacks no other neurologic deficits occurred. Cranial nerve damage could not be avoided in 21 cases (nervus recurrens, 7; nervus glossopharyngeus, 16; and nervus facialis, 4) but disappeared clinically within a 1- to 6-month period in all but two. Each surgical patient underwent control angiography, which demonstrated 30 arteries to be patent, two became occluded, and one had an insignificant stenosis. We conclude that standard surgical techniques are unsuitable for repair of highly located lesions of the ICA. Although extracranial-intracranial anastomosis has been proposed in patients with planned ligation of the ICA, the anatomic reconstruction remains advantageous because flow is restored to normal and the source of emboli is eliminated. With the use of a special approach, graft replacement can be performed up to the base of the skull. (J VASC SURG 1984;1:734-743.)