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1/4. Evaluation of progression and spread of atherothrombosis.

    Symptomatic atherothrombosis in one vascular bed is usually indicative of disseminated disease. Indeed, involvement of multiple beds is common in everyday clinical practice, and these patients are at much higher risk of ischaemic events. The prevention of manifestations following atherothrombosis is therefore an important therapeutic goal in these patients. Some causative risk factors demonstrate affinities to particular arterial domains. Cigarette smoking, for example, is particularly associated with atherothrombotic involvement of the pelvic and lower limb arteries, whereas arterial hypertension is associated with the intracranial cerebral arteries. The degree, spread and progression of atherosclerosis can be assessed using various non-invasive and invasive modalities: high-resolution Doppler ultrasound, ankle-brachial index (ABI) measurement, magnetic resonance (MR), computed tomography (CT) and intra-arterial angiography. Indicators of atherothrombotic risk include increased carotid artery intima-media thickness, microembolic signals on transcranial Doppler ultrasonography and low ABI. There is a strong rationale for the inclusion of the ABI measurement as part of the routine clinical examination to assess the cardiovascular risk in patients with identified risk factors. Furthermore, detection of a low ABI should serve as a trigger for patient management with aggressive antiplatelet therapy. The generalized nature of atherothrombosis and the methods for evaluating the spread of disease are illustrated through the case history of a patient with disseminated atherothrombotic disease.
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2/4. Pure or predominantly sensory transient ischemic attacks associated with posterior cerebral artery stenosis.

    Pure or predominantly sensory transient ischemic attacks (ps-TIAs) are uncommon, and underlying vascular abnormalities have rarely been described. The author reports 5 patients with TIAs which were of short duration, stereotypical and purely or predominantly sensory in nature. brain MRI did not reveal any lesions, while angiography demonstrated focal stenoses in the proximal portion of the posterior cerebral artery (PCA). It is concluded that ps-TIAs strongly suggest the presence of PCA disease. Repeated compromise of small vessels supplying the posterior-lateral part of the thalamus seems to be the pathogenic mechanism.
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3/4. Capsular infarcts: the underlying vascular lesions.

    In ten patients, 11 infarcts involving mainly the internal capsule have been examined pathologically. Serial sections of the involved basal ganglia were studied in ten infarcts and only a gross dissection was made in the other. The implicated penetrating arteries were traced throughout their length and obstructive vascular lesions were found in nine instances. In two of the nine there was an atheromatous plaque with a superimposed thrombus, in four an atheromatous plaque had caused severe stenosis, in one a destructive arterial process lipohyalinosis had occurred, in one case the nature of the obstruction remained "uncertained," and in one the penetrating arteries were obstructed at their orifices by an atheroma in the superior division of the middle cerebral artery. In two cases the vessels were patent, suggesting embolism. The atheromas consisted almost exclusively of a conglomerate of fat-filled macrophages. The clinical correlate was a pure motor hemiplegia or hemiparesis involving the face, arm, and leg without sensory deficit, homonymous hemianopia, receptive aphasia, or apractognosia. confusion was prominent in one patient.
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4/4. A neuropathological and neuropsychological study of Turner's syndrome.

    A neuropathological study was made in 2 women with Turner's syndrome. Neuropsychological investigation in one of them correlated with what has previously been found in Turner's syndrome as well as with the localization of the most pronounced neuropathological aberration which was of atherosclerotic nature, most pronounced in the right temporo-parietal area. These findings as well as the findings of acidophile hypoplasia of the pituitary gland are discussed.
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