Cerebral venous thrombosis (CVT) is an uncommon disorder in the general population. At least 1 risk factor can be identified in 85% of patients with CVT. Because of the high frequency of thrombophilia among patients with CVT, screening for hypercoagulable conditions should be performed. Two pathophysiological mechanisms contribute to their highly variable clinical presentation. Four major syndromes have been described: isolated intracranial hypertension, focal neurological abnormalities, seizures, and encephalopathy. Cavernous sinus thrombosis represents the single CVT which produces a characteristic clinical syndrome. Head Computed Tomography is the most frequently performed imaging study, but Magnetic Resonance Imaging of the head combined with Magnetic Resonance venography are the most sensitive studies. Acute phase therapy for CVT focuses on anticoagulation, management of seizures, increased intracranial pressure, and prevention of cerebral herniation. The majority of patients have a complete or partial recovery, however they have an increased incidence of venous thromboembolism. Clinical and imaging follow-ups 3–6 months after diagnosis are recommended to assess for recanalization.
Part of the book: Ischemic Stroke of Brain
Intracranial atherosclerotic stroke differs from extracranial atherosclerotic stroke in many aspects, including risk factors and stroke patterns. It occurs in association with in situ thrombotic occlusion, artery-to-artery embolism, branch occlusion, and hemodynamic insufficiency. Intracranial atherosclerotic stenosis (ICAS) could have only been diagnosed by transcranial Doppler (TCD) and transcranial color-coded sonography (TCCS), which are burdened by a risk of bias, or catheter angiography (DSA), which, on the contrary, is very precise, but rarely it is done in clinical practice due to its invasiveness. Computed tomography angiography (CT-A) and magnetic resonance imaging angiography (MR-A) have increased the identification of ICAS in a wider stroke population.
Part of the book: New Insight into Cerebrovascular Diseases
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
Aphasia denotes an acquired central disorder of language, which alters patient’s ability of understanding and/or producing spoken and written language. The main cause of aphasia is represented by ischemic stroke. The language disturbances are frequently combined into aphasic syndromes, contained in different vascular syndromes, which may suffer evolution/involution in the acute stage of ischemic stroke. The main determining factor of the vascular aphasia’s form is the infarct location. Broca’s aphasia is a non-fluent aphasia, comprising a wide range of symptoms (articulatory disturbances, paraphasias, agrammatism, anomia, and discrete comprehension disorders of spoken and written language) and is considered the third most common form of acute vascular aphasia, after global and Wernicke’s aphasia. It is caused by a lesion situated in the dominant cerebral hemisphere (the left one in right-handed persons), in those cortical regions vascularized by the superior division of the left middle cerebral artery (Broca’s area, the rolandic operculum, the insular cortex, subjacent white matter, centrum semiovale, the caudate nucleus head, the putamen, and the periventricular areas). The role of this chapter is to present the most important acquirements in the field of language and neurologic examination, diagnosis, and therapy of the patient with Broca’s aphasia secondary to ischemic stroke.
Part of the book: Aphasia Compendium