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