Evaluation and managment of CVT (Continuum).pdf

Purpose of Review: Thrombosis of the dural sinus and/or cerebral veins (CVT) is a rare but potentially devastating type of stroke that tends to occur in young adults, especially women. In this article, the abbreviation CVT refers to either cerebral venous thrombosis or dural sinus thrombosis. The purpose of this review is to review the most up-to-date literature on the epidemiology, diagnosis, management, and prognosis of CVT. In addition, illustrative cases that represent the spectrum of CVT are provided. Recent Findings: CVT represents about 0.5% of all strokes and can be challenging to diagnose because headache, rather than focal neurologic symptoms, is the prominent feature. The diagnosis is confirmed with MRI and magnetic resonance venogram (MRV). The mainstay of acute management is anticoagulation, although, in the cases of severe hemorrhagic conversion of a venous infarction, endovascular mechanical thrombectomy may be potentially lifesaving. The evaluation of underlying causes from transient triggers, eg, pregnancy, oral contraceptives, or infection, versus chronic triggers, eg, cancer and thrombophilia, will often influence the duration of anticoagulation. The outcomes after CVT are generally favorable, and the risk of recurrence is low. Summary: CVT is an important diagnosis to keep in mind when evaluating patients with headache in the emergency department, and it is important that it not be overlooked because it is treatable. Continuum (Minneap Minn) 2014;20(2):335–351. EPIDEMIOLOGY AND PATHOGENESIS Thrombosis of the dural sinus and/or cerebral veins (CVT) is relatively rare, accounting for only about 0.5% of patients with stroke and with a prevalence of only 5 per 1 million. CVT is also primarily a stroke type that affects individuals younger than the age of 50. In the 624 cases included in the International Study of Cerebral Venous Thrombosis (ISCVT), the median age was 37 years. The incidence of CVT in children is 0.67 per 100,000 per year, with 43% occurring in neonates. In addition, women make up about 75% of those with CVT, likely a result of the sex-specific risk factors that occur in women, including oral contraceptives, pregnancy, and hormone therapy use. CVT causes dysfunction by two mechanisms. (1) Thrombosis of cerebral veins causes localized edema of the brain and venous infarction. (2) Thrombosis of the major sinuses leads to intracranial hypertension as a result of increased venous pressure and impaired absorption of CSF. Generally, some underlying trigger or predisposing risk factor that increases the risk of thrombosis is the reason for the timing and occurrence of CVT. In the Address correspondence to Dr Cheryl Bushnell, Wake Forest School of Medicine, Department of Neurology, Medical Center Boulevard, Winston Salem, NC 27157, cbushnel@wakehealth.edu. Relationship Disclosure: Dr Bushnell has received grants from the Hazel K. Goddess Fund for Stroke Research in Women, the North Carolina Stroke Care Collaborative, the World Federation of Neurology, and the World Stroke Organization. Dr Saposnik is supported by the Distinguished Clinician Scientist Award from the Heart and Stroke Foundation of Canada. Unlabeled Use of Products/Investigational Use Disclosure: Drs Bushnell and Saposnik report no disclosures. * 2014, American Academy of Neurology. 335 Continuum (Minneap Minn) 2014;20(2):335–351 www.ContinuumJournal.com Review Article Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. ISCVT, 85% of patients with CVT had at least one identifiable risk factor for thrombosis and 44% had multiple predisposing factors. These predisposing factors are discussed in detail below. CLINICAL PRESENTATION The presentation of patients with CVT may be variable. It can be categorized into four clinical syndromes: (1) isolated intracranial hypertension (eg, patients may present with headache, diplopia, visual impairment [severe papilledema], decreased level of consciousness, or sixth nerve palsy), (2) focal neurologic deficit (eg, motor weakness, sensory deficit, aphasia), (3) encephalopathy, and (4) seizures (accompanied or not by a focal neurologic deficit). Headache is the most common symptom, affecting approximately 90% of patients with CVT. Isolated headaches are less common, butmay constitute a clinical challenge (Table 5-1). The presentation of headache associated with focal symptoms or seizures may suggest the presence of a venous infarction. Hemorrhagic conversion was reported in 35% to 39% of patients. Demographic characteristics associated with hemorrhagic conversion include older age, female sex, and an acute onset (48 hours). Themost commonly affected venous sinus is the superior sagittal (62%) followed by the transverse sinus (41% to 45%; Figure 5-1). Patients less commonly present with deep cerebral venous occlusion of the internal cerebral vein or vein of Galen (11%), or straight sinus (18%), but they are at a nearly threefold higher risk of death and dependency during follow-up. These patients may present with bilateral thalamic or basal ganglia infarction, and will often have decreased level of consciousness and rapid neurologic deterioration. Some symptoms may guide the localization or extension of the CVT. For example, patients with deep cerebral venous occlusion or extensive CVT (involving the superior sagittal plus other sinuses) may present with decreased level of consciousness with bilateral papilledema. The development of headaches and fever in the context of an underlying otitis or sinusitis may raise suspicion about CVT involving the transverse or sigmoid sinuses. Delays in diagnosis are common, likely related to an insidious course in up to two-thirds of patients.

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