Varicella with delayed hemiplegia

We report 4 children who developed acute hemiplegia 7 weeks to 4 months after varicella infection. In 2 patients, carotid angiography demonstrated segmental narrowing and occlusion of the middle cerebral artery. Their clinical and angiographic features were similar to those associated with contralateral hemiplegia after herpes zoster ophthalmicus, the pathogenesis of which comprises cerebral angiitis due to varicella zoster viral infection. We believe that our patients had the same pathogenesis. In a survey of infectious diseases in our region, the frequency of varicella with delayed hemiparesis was roughly 1:6,500 varicella patients.     

Herpes zoster ophthalmicus followed by contralateral hemiparesis: report of two cases and review of literature.

Two patients with herpes zoster ophthalmicus and contralateral hemiparesis are described, and their findings compared with 49 patients previously reported. These patients presented with delayed contralateral hemiparesis approximately seven weeks after the onset of herpes zoster ophthalmicus. Most patients had evidence of infarction of the ipsilateral middle cerebral artery by angiography or by CT scan. Cerebrospinal fluid pleocytosis and elevated protein commonly were found. Twenty per cent of the reported patients died, but they were older than the patients who survived and predisposed to have diffuse CNS lesions. The pathogenesis of this syndrome is thought to be due to direct viral invasion of the blood vessel wall with resulting angiitis. Further studies need to be performed to clarify the role of specific antiviral therapy or anti-inflammatory agents in treating this complication of herpes zoster.     

Granulomatous angiitis following primary varicella zoster infection

Granulomatous angiitis is an uncommon but well recognized complication of varicella zoster infection. The classic presentation is of a delayed hemiparesis in an often immunocompromised patient following zoster ophthalmicus. This report outlines the case of a young woman who developed a large left middle cerebral artery territory infarct secondary to granulomatous angiitis during primary varicella zoster infection.     

Angiographic findings in herpes zoster arteritis

Four adults patients who experienced an ipsilateral hemispheric deficit 6 to 8 weeks after having developed herpes zoster ophthalmicus were seen during a six-month period. All four patients underwent full-circle angiography, including study of the extracranial arteries in the three older patients. Each examination demonstrated areas of segmental constriction of arteries on the ipsilateral side; two locations that were especially affected were the A2 segment of the pericallosal artery beneath the genu of the corpus callosum and the M4 segment of the middle cerebral artery. The cerebral arteries of the opposite hemisphere and the extracranial vessels did not contain demonstrable abnormalities. Pathological studies suggest that patients with this syndrome may have a necrotizing arteritis of ipsilateral blood vessels; in patients with disseminated zoster, a granulomatous angiitis of cerebral blood vessels has been found. We propose that the pattern of angiographic abnormalities described here is characteristic of herpes zoster arteritis; furthermore, the distribution pattern of the lesions suggests that the virus may spread to these arteries via branches of the ophthalmic division of the trigeminal nerve.     

Varicella with delayed contralateral hemiparesis detected by MRI

We report a 3 1/2-year-old boy who developed a hemiparesis 4 weeks after the onset of a varicella infection. In previously described cases of varicella with delayed contralateral hemiparesis, computed tomography typically revealed infarcts in the basal ganglia and internal capsule. To our knowledge, our patient is the first studied by magnetic resonance imaging. The pathogenesis of this syndrome may be a varicella zoster virus-related vasculopathy similar to that observed in herpes zoster ophthalmicus with delayed contralateral hemiparesis.     

Acute hemiplegia associated with herpes zoster infection in children: report of one case

Herpes zoster infection has been rarely reported to cause angiitis of the central nervous system in children. We describe a 4-year, 8-month-old female with acute hemiplegia and central facial palsy 6 weeks after she had had zoster ophthalmicus. The findings of magnetic resonance angiography, the clinical picture, and a preceding history of herpes zoster ophthalmicus suggested zoster vasculitis. Herpes zoster vasculitis is thus another consideration when examining a child with acute hemiplegia and a recent herpes zoster infection.     

Cerebral vasculopathy associated with primary varicella infection

A previously healthy 5-year-old boy developed cerebral vasculopathy, presenting as two episodes of acute hemiparesis 3 and 9 months, respectively, after a primary varicella infection (chickenpox). This association has not been reported before, to our knowledge, although cerebral vasculopathy is a well-known complication of herpes zoster ophthalmicus. The diagnosis was based on the presence of oligoclonal varicella-specific IgG in the cerebrospinal fluid and angiographic findings. Clinical and angiographic follow-up, and serial thymidine kinase activity levels in the cerebrospinal fluid suggested a self-limiting course of the virus-induced vasculopathy. Varicella zoster virus seems to be another potential causative agent to be considered in acute childhood hemiplegia.     

Herpes zoster ophthalmicus with delayed cerebral infarction and meningoencephalitis

Herpes zoster ophthalmicus can be complicated by a delayed ipsilateral cerebral angiitis which may cause infarction and a smoldering meningoencephalitis. We describe such a case treated successfully with steroids and acyclovir. It is important to consider the diagnosis of this disorder early since therapeutic intervention may prevent an otherwise high morbidity and mortality. Steroids may have to be continued for some time after clinical resolution, using the ESR as a guideline for decreasing dosages.     

Stroke after zoster ophthalmicus in a 12-year-old girl with protein C deficiency.

A 12-year-old girl who had zoster ophthalmicus 10 months earlier presented with hemiparesis and corresponding basal ganglionic infarction related to middle cerebral artery branch thrombosis ipsilateral to the zoster. Hematologic evaluation disclosed protein C deficiency. This represents the first zoster-associated stroke reported in childhood associated with protein C deficiency, with extension of the latency period between zoster and infarction, previously reported to be 6 months.     

Acute hemiplegia with lacunar infarct after varicella infection in childhood

We report 4 cases of acute hemiplegia and a small low-density lesion on computerized tomography (CT) after varicella infection. In 3 of them, CT in the acute hemiplegic stage, and later, reveals the development of lacunar infarct around the internal capsule. Focal low density may be caused by occlusive vascular lesions of the penetrating arteries. Varicella infection may play an important role as one of the causes of acute hemiplegia in childhood producing lacunar infarct, as well as delayed hemiplegia, reported previously in herpes zoster ophthalmicus.     

A case of delayed cerebral infarction occurring in puerperium preceded by herpes zoster ophthalmicus in late pregnancy]

Delayed central neurological symptoms following herpes zoster ophthalmicus (HZO) such as "herpes zoster ophthalmicus and delayed contralateral hemiparesis" are considered to be due to ipsilateral intracranial vasculopathy. We experienced a rare case with cerebral infarction occurred in puerperium following HZO in late pregnancy. A healthy 30-year-old woman had left HZO at weeks 35 of gestation. She was given acyclovir (ACV) for external use and improved with small pigmentation on the left eye-lid. Seven weeks after the onset of HZO, she suddenly developed aphasia and right hemiparesis. Cerebral angiogram showed narrowing on M 1 segment of the ipsilateral middle cerebral artery. The occlusion was seen on peripheral portion of the angular artery on the same side. In cerebrospinal fluid (CSF), cell count was slightly elevated, but concentration of protein and sugar were normal. Varicella-zoster titer was increased in both serum and CSF. She was treated with intravenous ACV (1500 mg/day) for 10 days. On the next day after the treatment, the cell count was normalized and on 18th day, varicella-zoster titer was decreased in CSF. Higher brain function improved and no relapses occurred. This is a first case of delayed cerebral infarction occurring in puerperium preceded by herpes zoster ophthalmicus in late pregnancy, as far as we searched. We should treat carefully pregnant or lactating patients with HZO, considering delayed cerebral infarction.     

Cervical herpes zoster and delayed brainstem infarction.

Varicella-zoster (VZ) virus is a rare cause of CNS angiitis, which commonly presents as herpes zoster ophthalmicus with contralateral hemiplegia due to hemispheric infarction. We report the first case of VZ-angiitis with infarction in the ventral pons, following cervical herpes zoster.     

Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction

We studied five patients who had acute cerebral infarctions 5 weeks to 6 months after herpes zoster ophthalmicus (HZO). All had infarcts of the cerebral hemisphere ipsilateral to the HZO, and one also had a cerebellar infarct. Cerebral arteriography in one patient disclosed narrowing of the middle cerebral artery, occlusion of the anterior cerebral artery ipsilateral to the HZO and narrowing of the opposite anterior cerebral artery. In another case, arteriography revealed occlusion of the distal internal carotid artery on the side of the HZO.     

Hemichorea caused by intracranial hemorrhage following contralateral herpes zoster ophthalmicus

A healthy, 66-year-old, right-handed man was admitted to our university hospital and diagnosed with herpes zoster ophthalmicus (HZO). After 4 weeks, he complained of hemichorea on his left side. Brain MRI showed a focal hemorrhage in the right subthalamic area. No evidence of aneurysmal lesion or cerebral angiitis was observed on cerebral angiography.     

Postvaricella acute transverse myelitis in a previously vaccinated child

We describe a 14-year-old boy with acute transverse myelitis after breakthrough varicella infection, despite immunization with the Varicella zoster virus vaccine 8 years earlier. He recovered fully after treatment with intravenous corticosteroids and acyclovir. To our knowledge, there are no previously reported cases of postvaricella acute transverse myelitis in vaccinated individuals. Our report emphasizes that the Varicella zoster virus booster vaccine may be necessary to prevent not only acute varicella, but also its postinfectious neurologic complications.     

Encephalomyelitis and demyelinating diseases in patients with extracerebral malignant tumors

We examined central nervous system (CNS) lesions in 456 patients with primary extracerebral malignant tumors. Inflammatory reactions caused by viral (progressive multifocal leukoencephalopathy (PML), herpes zoster varicella), fungal, or bacterial infections could be demonstrated in 20 patients. In a further 19 patients, the brain tissue showed lymphocyte infiltrates of unknown etiology and, in four of these, autopsy revealed probable paraneoplastic, non-bacterial, endocarditis as a possible explanation for the local inflammatory reaction. The frequency of thrombophlebitis, non-arteriosclerotic thrombosis and arteritis was significantly higher than in a control group of 2052 tumor-free patients. Focal spongiform-axonopathic lesions (24 cases) as well as diffuse leukoencephalopathy (11 cases) were interpreted as probably being at least in part paraneoplastic because the same alterations could also be observed in patients who had never undergone cytostatic or radiation therapy. The possible pathogenetic conditions are discussed and a classification of these tumor-accompanying, but not always tumor-dependent, lesions suggested.     

Multifocal varicella-zoster virus leukoencephalitis temporally remote from herpes zoster

Two patients with cancer, one with Hodgkin's disease and the other with a granulosa cell tumor of the ovary, developed a progressive, eventually fatal infection of the central nervous system exhibiting multifocal symptoms and signs. Pathologically, gross abnormalities of the brain resembled those in progressive multifocal leukoencephalopathy (PML), with discrete and confluent plaque-like lesions concentrated in the white matter, particularly along the gray-white junction. Microscopically, pathological changes differed distinctly from those associated with PML; in addition to confluent foci of white matter injury characterized by early demyelination and subsequent necrosis, prominent Cowdry type A eosinophilic intranuclear inclusions were noted in oligodendrocytes, astrocytes, and neurons. By electron microscopy, intranuclear spherical particles consistent in size and appearance with herpesvirus nucleocapsids were found within the lesions. Immunoperoxidase studies detected varicella-zoster virus (VZV) antigens in infected cells, implicating this virus as the responsible agent despite a lapse of many months between the cutaneous herpes zoster and onset of cerebral symptoms in both patients.     

Transient contralateral hemiplegia after ophthalmic zoster. Therapeutic problems in elderly patients

Summary Delayed ipsilateral carotid arteritis is a known complication of herpes zoster ophthalmicus. The case of a 70-year-old man with two TIAs following ophthalmic zoster is reported, and the therapeutic problems in elderly patients are discussed.

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Zusammenfassung Homolaterale, verspätete Karotis-Arteriitis ist eine bekannte Komplikation des Herpes Zoster Ophthalmicus. Es wird über einen 70jährigen Mann berichtet, bei dem zwei TIA nach Zoster Ophthalmicus auftraten. Therapeutische Probleme werden diskutiert.

     

Acute, chronic, and recurrent varicella zoster virus neuropathy without zoster rash

The authors report three patients with acute, chronic, and recurrent neuropathy associated with varicella zoster virus (VZV) infection but without zoster rash. CSF of all three patients contained VZV immunoglobulin G antibody, but not herpes simplex virus. In two patients, serum/CSF ratios of VZV immunoglobulin G were reduced compared to normal ratios for immunoglobulin G and albumin, and one patient also had VZV immunoglobulin M in CSF. All three patients received antiviral therapy and improved. The diagnosis of nervous system infection by VZV may be confirmed by the presence of antibody to VZV in CSF even without detectable VZV DNA.     

Infantile herpes zoster ophthalmicus and acute hemiparesis following intrauterine chickenpox

A 17-month-old boy developed herpes zoster ophthalmicus (HZO) and delayed contralateral hemiparesis following intrauterine varicella exposure. CT demonstrated multiple areas of hypodensity in the left basal ganglia, and angiography showed occlusion of left lenticulostriate arteries. As in most adults with HZO and delayed hemiparesis, this infant had a self-limiting course with excellent recovery.