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1、 Vol 8 August 2009 731ReviewVaricella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatmentDon Gilden, Randall J Cohrs, Ravi Mahalingam, Maria A NagelVasculopathies caused by varicella zoster virus (VZV) are indicative of a productive virus in
2、fection in cerebral arteries after either reactivation of VZV (shingles) or primary infection (chickenpox). VZV vasculopathy can cause ischaemic infarction of the brain and spinal cord, as well as aneurysm, subarachnoid and cerebral haemorrhage, carotid dissection, and, rarely, peripheral arterial d
3、isease. VZV vasculopathy in immunocompetent or immunocompromised individuals can be unifocal or multifocal with deep-seated and superficial infarctions. Lesions at the greywhite matter junction on brain imaging are a clue to diagnosis. Involvement of both large and small arteries is more common than
4、 that of either alone. Most patients have a mononuclear cerebrospinal fluid pleocytosis, often with red blood cells. Cerebrospinal fluid pleocytosis and rash are absent in about a third of cases. Anti-VZV IgG antibody in the cerebrospinal fluid is found more frequently than VZV DNA. In recent years,
5、 the number of recognised VZV vasculopathies has grown, and accurate diagnosis is important for the effective treatment of these disorders. Introduction Primary VZV infection, which usually occurs in children, results in chickenpox (varicella), after which the virus becomes latent in ganglionic neur
6、ons along the entire neuraxis. Years later, as cell-mediated immunity to VZV declines with age or from immunosuppression (such as in organ-transplant recipients or patients with cancer or AIDS), VZV can reactivate to cause zoster (shingles). Zoster is often followed by chronic pain (postherpetic neu
7、ralgia), as well as vasculopathy, myelopathy, retinal necrosis, and cerebellitis (figure 1). VZV reactivation can also cause pain without rash (zoster sine herpete); in fact, all neurological complications of VZV reactivation can occur without rash. Over the past few decades there has been an increa
8、sing number of reports of vascular disease after VZV reactivation. Unlike early cases of acute hemiplegia after contralateral zoster caused by large-artery disease, the recognised clinical range of this disease has expanded to include transient ischaemic attacks and protracted illness involving both
9、 small and large arteries. In addition to ischaemic infarction, VZV can cause aneurysm, cerebral and subarachnoid haemorrhage, and arterial ectasia, and might be a co-factor, along with trauma, in the pathogenesis of cerebral arterial dissection. Furthermore, VZV can also cause peripheral arterial d
10、isease. In adults, the exact incidence of VZV vasculopathy is difficult to estimate, although it is more common in immuno compromised individuals. In children, VZV vasculopathy has been proposed to account for 31% of all arterial ischaemic strokes;1 moreover, stroke was preceded by chickenpox in 44%
11、 of children with transient cerebral arteriopathy.2 In this Review, we outline the ever-widening spectrum of vascular disease after VZV reactivation (zoster), as well as after primary infection (varicella), and discuss the underlying mechanisms of the disease. We also emphasise the importance of acc
12、urate diagnosis to enable appropriate treatment of VZV vasculopathies.History The earliest recorded description of VZV vasculopathy was about 50 years ago when Cravioto and Feigin3 described what they believed was “a non-infectious granulomatous angiitis with a predilection for the nervous system, c
13、haracterized by thrombosis in cerebral arteries and distinguished from other vasculitides by the nature of the inflammatory response, which consisted predominantly of histiocytes, mononuclear cells and multinucleated giant cells”. Years later, Rosenblum and Hadfield4 described granulomatous angiitis
14、 of the nervous system in patients with herpes zoster and lymphosarcoma, characterised by infiltrates of mono- nuclear cells and multinucleated giant cells in cerebral arteries. The first angiographic studies of the large arteries in the neck and intracranial arteries in a patient with herpes zoster
15、 ophthalmicus and delayed contralateral hemiparesis revealed segmental arteritis in the area of the carotid siphon.5 Until recently, these older cases of VZV vasculopathy were described as granulomatous angiitis, VZV vasculitis, or zoster ophthalmicus and delayed contralateral hemiparesis, although
16、VZV vasculopathy can occur after zoster anywhere in the body.Clinical features and diagnosis Clinical presentation Although early case reports emphasised that patients present with acute stroke, many patients have transient ischaemic attacks with protracted neurological symptoms and signs. Common clinical features are not limited to acute hemiplegia and include headache, changes in mental status, aphasia
