Aphasia represents an acquired central disorder of language that impairs a person’s ability to understand and/or produce spoken and written language, caused by lesions situated usually in the dominant (left) cerebral hemisphere, in right-handed persons. Aphasia has a prevalence of 25–30% in acute ischemic stroke (vascular aphasia). It is considered as an important stroke severity marker, being associated with a higher risk of mortality, poor functional prognosis, and augmented risk of vascular dementia. The assessment of aphasias in clinical practice is based on classical analysis of oral production and comprehension. The language disturbances are frequently combined into aphasic syndromes which are components of different vascular syndromes that may evolve/involve rapidly at the acute stage of ischemic stroke. The main determinant of the type of vascular aphasia is the infarct location (especially left middle cerebral artery territory). Recent studies at the hyperacute stage of ischemic stroke have observed features of aphasia, have reanalyzed its neuroanatomy using new imaging techniques, and have shown that aphasias have a parallel course to that of cortico-subcortical hypoperfusion. Thus, the reversal of hypoperfusion, following recanalization (spontaneous or secondary to thrombolysis or thrombectomy), is associated with resolution of aphasia. Speech therapy is needed as soon as permitted by clinical condition.
Part of the book: Ischemic Stroke
Giant cell arteritis (GCA) is a primary vasculitis that affects especially extracranial medium-sized arteries, such as superficial temporal arteries (TAs). Three findings are important for the ultrasound (US) diagnosis of TA: „dark halo” sign, which represents vessel wall edema, stenosis, and acute occlusions. US has a high sensitivity to detect vessel wall thickening in the case of large vessels GCA. The eye involvement in GCA is frequent and consists in arteritic anterior ischemic optic neuropathies or central retinal arterial occlusion, with abrupt, painless, and severe loss of vision of the involved eye. Because findings of TAs US do not correlate with eye complications in GCA, color Doppler imaging of the orbital vessels is of critical importance (it reveals low end diastolic velocities, and high resistance index), in order to quickly differentiate the mechanism of eye involvement (arteritic, versus non-arteritic). The former should be treated promptly with systemic corticosteroids to prevent further visual loss of the fellow eye.
Part of the book: Giant-Cell Arteritis