Search

Introduction: This study aimed to analyze the risk factors for varicella encephalitis in children and establish a predictive model., Methods: This retrospective cohort study included a varicella encephalitis group ( n = 75) and a varicella-non-encephalitis group ( n = 135). Logistic regression analysis was employed to find risk factors for varicella encephalitis and create a predictive model., Results: Older age, vomiting, poor mental status, and prolonged rash duration were independent risk factors for varicella encephalitis ( p < .05). The predictive model for varicella encephalitis combined above four factors. The ROC curve of the predictive model showed an area under the curve of 0.955 (95% CI 0.925-0.986) for varicella encephalitis in children with a sensitivity of 94.7%, and a specificity of 86.0%., Conclusion: Children with varicella who are older, experience vomiting, exhibit poor mental status, or have a prolonged rash duration should be closely monitored clinically. The predictive model combining these four factors demonstrates good predictive efficiency., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: There are established associations between viral and autoimmune encephalitis as well as between autoimmune encephalitis and demyelinating central nervous system (CNS) diseases. Here, we report the evolution from varicella zoster virus (VZV) encephalitis to limbic autoimmune encephalitis (AIE) to multiple sclerosis (MS) in one patient., Case Report: A woman in her mid-thirties presented with headache, aphasia, and a generalized tonic-clonic seizure. Cerebrospinal fluid (CSF) VZV polymerase chain reaction was positive and treatment with acyclovir was administered for VZV encephalitis. Five months later, the patient presented with cognitive deficits and MRI showed new bilateral hippocampal T2-hyperintensities. CSF analyses revealed pleocytosis and neuropil antibodies in tissue-staining. A diagnosis of limbic AIE was established and treatment with IV steroids and IV immunoglobulins initiated. One year later, the patient developed paresthesia of both legs and magnetic resonance imaging studies now showed new supratentorial and spinal demyelinating lesions. The patient was diagnosed with MS and treatment was changed to rituximab., Conclusions: This unique case report links three important neuroimmunological entities in characterizing the evolution from infectious to autoimmune encephalitis to multiple sclerosis in one patient. Identification of such rare clinical constellations is critical for correct treatment choice and provides important novel insights into the pathophysiology of neuroimmunological disorders including viral triggers and overlap manifestations of autoimmune CNS diseases., (© 2024. The Author(s).)

Competing Interests: The authors report no conflicts of interest.

Encephalitis is inflammation of the brain parenchyma, most often caused by viruses. Historically, data have shown herpes simplex virus 1 and 2 to be the most common causes of viral encephalitis, with cases due to varicella zoster virus (VZV) more often seen in older age and immunocompromised states. However, emerging data show VZV as an increasingly common culprit of encephalitis in young, immunocompetent patients. PCR analysis of the cerebrospinal fluid is the most accurate diagnostic modality for viral encephalitis. Appropriate and complete treatment hinges on accurate identification of the cause of encephalitis, underscoring the need for comprehensive testing. We present a case of VZV encephalitis in an immunocompetent male patient in his 40s., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Vedolizumab is a monoclonal antibody that has demonstrated efficacy and a good safety profile in patients with inflammatory bowel disease. Varicella zoster virus encephalitis is a potentially serious complication not previously described with its use, highlighting the importance of vaccination, as well as early diagnosis and treatment of infections in this type of patients.

Objective: To investigate the clinical and magnetic resonance imaging (MRI) characteristics of patients with varicella zoster virus (VZV) reactivation involving the cranial nerves and central nervous system (CNS)., Methods: This is a retrospective, multi-center case-series of 37 patients with VZV infection affecting the cranial nerves and CNS., Results: The median age was 71 years [IQR 51.5-76]; 21 (57%) were men. Cerebrospinal fluid (CSF) was available in 24/37 (65%); median CSF white blood cell count was 11 [IQR 2-23] cells/μL and protein was 45.5 [IQR 34.5-75.5] mg/dL. VZV polymerase chain reaction (PCR) assays were positive in 6/21 (29%) CSF and 8/9 (89%) ocular samples. Clinical involvement included the optic nerve in 12 (32%), other cranial nerves in 20 (54%), brain parenchyma in 12 (32%) and spinal cord or nerve roots in 4 (11%). Twenty-seven/28 immunocompetent patients' MRIs were available for review (96%). Of the 27, 18 had T1 postcontrast fat saturated sequences without motion artifact to evaluate for cranial nerve enhancement and optic perineuritis (OPN). Eight/18 (44%) demonstrated OPN. All 8 experienced vision loss: 3 optic neuritis, 1 acute retinal necrosis, and 3 CNS vasculitis with 1 central and 1 branch retinal artery occlusion and 1 uveitis. Diplopic patients had cranial nerve and cavernous sinus enhancement. All immunosuppressed patients were imaged. Seven/9 (88%) had extensive neuraxis involvement, including encephalitis, vasculitis and transverse myelitis; one case had OPN., Conclusion: OPN is a frequent manifestation in VZV-associated vision loss among immunocompetent patients. Immunosuppressed patients had greater neuraxis involvement. Optimizing MRI protocols may improve early diagnosis in VZV reactivation., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Varicella-zoster virus (VZV) lurks in cranial nerves and other brain ganglias after infection. Because middle cerebral artery (MCA) receives the ipsilateral trigeminal ganglia afferent innervations, the reactivated VZV infects the adventitia and intima of cerebral artery wall probably through this way and causes vascular inflammation, finally resulting in artery remodeling, vessel occlusion, and ischemia. In fact, there is a growing clinical recognition that there is an association between VZV reactivation and subsequent stroke. Here, we showed a case of ischemic stroke secondary to varicella-zoster virus meningoencephalitis and reviewed the literature to emphasize the importance of VZV-associated vasculopathy., (© 2022. Journal of NeuroVirology, Inc.)

Varicella-zoster virus (VZV) is one of the most common agents causing viral infections of the central nervous system (CNS). VZV encephalitis is associated with severe neurological sequelae, despite antiviral treatment. Cognitive impairment has been reported and VZV has been associated with dementia. Our aim was to investigate the cognitive impairment and cerebrospinal fluid biomarkers in a follow-up study of patients with VZV encephalitis. Thirteen patients with VZV encephalitis, diagnosed by detection of VZV DNA in cerebrospinal fluid (CSF) by PCR and concomitant symptoms of encephalitis, were included. Neuropsychological assessment in parallel with a lumbar puncture to obtain CSF was performed 1.5-7 years after acute disease. The CSF biomarkers neurofilament light chain (NFL), S100B, glial fibrillary acidic protein (GFAP), amyloid-β (Aβ) 40 and Aβ42, total tau (t-tau) and phosphorylated tau (p-tau) were analysed and compared to controls (n = 24). Cognitive impairment was shown in the domains of executive functions and speed/attention and to a minor degree in the domains of learning/memory and language, indicated by a significantly poorer performance on seven neuropsychological test variables. No convincing evidence of alterations in concentrations of biomarkers in the CSF were shown. Our results indicate that patients with VZV encephalitis suffer from cognitive impairment long time after acute disease. Importantly, these impairments do not seem to be accompanied by biomarker evidence of ongoing neuronal or astrocytic injury/activation or induction of dementia-related brain pathologies by the infection.

Immunosuppressed patients are at higher risk for developing herpes zoster (HZ), and neurological complications are frequent in them. However, the influence of immunosuppression (IS) on the severity and prognosis of neurological complications of varicella-zoster virus (VZV) reactivation is unknown. We studied retrospectively patients with neurological complications due to VZV reactivation who attended our hospital between 2004 and 2019. We aimed to assess the clinical spectrum, potential prognostic factors, and the influence of the immune status on the severity of neurological symptoms. A total of 98 patients were included (40% had IS). Fifty-five patients (56%) had cranial neuropathies which included Ramsay-Hunt syndrome (36 patients) and cranial multineuritis (23 patients). Twenty-one patients developed encephalitis (21%). Other diagnosis included radiculopathies, meningitis, vasculitis, or myelitis (15, 10, 6, and 4 patients, respectively). Mortality was low (3%). At follow-up, 24% of patients had persistent symptoms although these were usually mild. IS was associated with severity (defined as a modified Rankin scale greater than 2) (odds ratio, 4.23; 95% confidence interval, 1.74-10.27), but not with prognosis. Shorter latency between HZ and neurologic symptoms was the only factor associated with an unfavorable course (death or sequelae) (odds ratio, 0.82; 95% confidence interval, 0.71-0.95). In conclusion, the clinical spectrum of neurological complications in VZV reactivation is wide. Mortality was low and sequelae were mild. The presence of IS may play a role on the severity of neurological symptoms, and a shorter time between HZ and the onset of neurological symptoms appears to be a negative prognostic factor.

Acute encephalitis can be life-threatening, especially in the immunocompromised population. Viruses are the main infectious agents, with varicella zoster virus (VZV) a common cause. Neuropsychiatric symptoms are well documented, but it is rare for mania to be the only symptom on presentation. Here, we report a case of hypomania in a 31-year-old white British heterosexual man who following investigation was found to be HIV positive and subsequently diagnosed with VZV encephalitis. To date, we are unaware of any similarly reported cases. It is important to raise awareness of atypical HIV presentations to improve clinical outcomes for patients., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Varicella zoster virus (VZV) is a pathogenic human herpes virus which causes varicella as a primary infection, following which it becomes latent in peripheral autonomic, sensory, and cranial nerve ganglionic neurons from where it may reactivate after decades to cause herpes zoster. VZV reactivation may also cause a wide spectrum of neurological syndromes, in particular, acute encephalitis and vasculopathy. While there is potentially a large number of coding viral mutations that might predispose certain individuals to VZV infections, in practice, a variety of host factors are the main determinants of VZV infection, both disseminated and specifically affecting the nervous system. Host factors include increasing age with diminished cell-mediated immunity to VZV, several primary immunodeficiency syndromes, secondary immunodeficiency syndromes, and drug-induced immunosuppression. In some cases, the molecular immunological basis underlying the increased risk of VZV infections has been defined, in particular, the role of POL III mutations, but in other cases, the mechanisms have yet to be determined. The role of immunization in immunosuppressed individuals as well as its possible efficacy in preventing both generalized and CNS-specific infections will require further investigation to clarify in such patients.

Varicella zoster virus (VZV) can invade the brainstem or brain via the glossopharyngeal, vagus , or facial nerve, resulting in brainstem inflammation or encephalitis. We report the case of a 66-year-old male patient with a primary manifestation of medulla injury of the glossopharyngeal and vagus nerves, combined with a medulla lesion, who was misdiagnosed with lateral medullary syndrome. Facial nerve injury and earache subsequently occurred and human herpes virus 3 (VZV) was detected by second-generation sequencing of the cerebrospinal fluid. The final diagnosis was varicella zoster encephalitis, which improved after antiviral therapy.

Background: Varicella-associated cerebral vasculopathy (VACV) is a serious complication of Varicella zoster virus (VZV) infection. VACV has protean manifestations, with varying clinical, radiological features and prognosis., Case Description: Moyamoya syndrome (MMS) with VACV is reported in few cases in the past. All the patients were in paediatric age group, presenting with multiple episodes of transient ischemic attacks (TIAs) and infarct. Our case was a 10-year-old Indian girl with ischemic stroke due to VACV who was treated with intravenous acyclovir. She presented 11 months later with multiple episodes of TIAs. Her angiogram showed bilateral moyamoya vasculature. Acetazolamide challenge study revealed areas of hypoperfusion. Previously reported such cases had been treated medically with steroids and antiplatelets. Most of these patients had resolution of motor symptoms after long follow-up; however, this period was marred by recurrent symptoms. Our patient underwent cerebral revascularisation procedure, following which her TIAs resolved, there was improvement in her limb power and, according to her parents, her performance in school has improved at 2-year follow-up., Conclusion: MMS can be a manifestation of VACV and should be suspected in paediatric patient of non-east Asian population. These patients require treatment with intravenous acyclovir to inactivate the virus. Those with TIAs should undergo cerebral revascularisation procedures. Medical management should be reserved for patients with adequate collaterals.

Rationale: The coexistence of Ramsay Hunt syndrome (RHS) and varicella-zoster virus (VZV) encephalitis is rare. A patient who developed RHS after being infected with VZV, along with a pontine lesion, is reported in the present study., Patient Concerns: A 41-year-old male patient presented with his mouth askew for 7 days, and dizziness, accompanied by hearing loss for 3 days., Diagnoses: The patient was initially diagnosed with RHS. Brainstem encephalitis was confirmed by lumbar puncture and cerebrospinal fluid. Brain magnetic resonance imaging (MRI) and diffusion-weighted imaging (DWI) revealed how VZV entered the intracranial space along the vestibulocochlear nerve and facial nerve in the acute period., Interventions: Intravenous acyclovir, IV, immunoglobulins (IVIg) and methylprednisolone were administered., Outcomes: The herpes was cleared up and left facial nerve palsy was improved, but hearing loss in the left ear did not improve., Lessons: An MRI was necessary for some VZV infections limited to the cranial nerve, although there was no evidence of brain stem injury. DWI provided evidence, showing how VZV entered the brain in the early stage. This allowed the doctor to judge the necessity of a lumbar puncture.

Varicella zoster virus (VZV) is less susceptible than herpes simplex virus to acyclovir. The optimal acyclovir regimen during VZV encephalitis remains unknown. We report two cases of acute renal failure after an increase in acyclovir dosage from 10 mg to 15 mg/kg/8 h during the treatment of VZV encephalitis according to French guidelines.

We report the case of a newly-diagnosed HIV-positive patient with varicella zoster virus aneurysmal vasculopathy confirmed on intrathecal antibody testing, despite a negative Cerebrospinal fluid (CSF) Varicella Zoster Virus (VZV) Polymerase Chain Reaction (PCR). This highlights the importance of prompt treatment with antiviral and steroid therapy in the presence of clinical or radiological suspicion whilst awaiting further confirmatory testing.

Background: We have reported the presence of varicella-zoster virus (VZV) DNA and viral particles in the cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients during exacerbation. It is not known whether these viruses are infective., Aim: To determine whether the VZV found in CSF of MS patients in exacerbation phase are infective., Methods: VZV found in CSF of MS patients was quantified by qPCR. Vero E6 cell cultures were incubated with CSF of five MS cases positive for VZV DNA, containing herpes-like viral particles. Propagated virus harvested from these cultures were used to infect new VeroE6 cells. Localization of an immediate-early and a late structural VZV proteins was monitored by confocal microscopy after 72 h. CSF from five non-inflammatory neurological (NIN) patients were used as controls., Results: A cytopathic effect was found in cultured cells inoculated with CSF from MS patients. Both, structural VZV glycoprotein (gB) and immediate-early VZV protein (IE62) were detected in Vero E6 cultures inoculated with samples from all five MS cases. CSF from control patients produced no effect on Vero E6 cells., Conclusion: When present in the CSF at relapses of MS, VZV is infective under in vitro conditions., (Copyright © 2018 IMSS. Published by Elsevier Inc. All rights reserved.)

In this case study, we summarise the inpatient investigations and management of a 68-year-old woman with Takotsubo cardiomyopathy secondary to a Varicella zoster encephalitis and the difficulties inherent with making this diagnosis. She presented with evolving cranial nerve neuropathies, which started with a vagal nerve mononeuritis and eventually included left-sided sensorineural hearing loss and a facial nerve palsy. These symptoms were concomitant with a variety of cardiac abnormalities, including fast atrial fibrillation and electrocardiographic changes. We summarise some of the current understanding of Takotsubo cardiomyopathy and the criteria for its diagnosis. Although left ventricular apical ballooning has been described in association with severe infections and states of high stress, we have not seen it reported in association with a Varicella zoster encephalitis., (© Royal College of Physicians 2017. All rights reserved.)

A 56-year-old immunocompetent male developed brainstem encephalitis complicating Ramsay Hunt syndrome. The disease had a slowly progressing course of months after the triggering infection, much longer than previously reported. Furthermore, magnetic resonance imaging, physical-chemical, and cell count analyses on cerebrospinal fluid were normal, whereas polymerase chain reaction for varicella zoster virus DNA was positive. The simultaneous negativity of both imaging and basic CSF exams is very rare, although possible event which confirms the irreplaceable role of viral screening on CSF. A systematic review of similar reports with highlights on the unusual aspects of our case is also presented.

Purpose: Survivors of viral encephalitis can develop refractory epilepsy and hippocampal sclerosis. Both the initial infectious insult and the secondary effects of recurrent seizures have been implicated in chronic disease progression. Recently, post-infectious autoimmunity, involved in acute relapses, has also been proposed as a pathomechanism for chronic disease progression. Our case series suggests a potential role of antibodies against the N-methyl-d-aspartate receptor (NMDAR) in chronic inflammatory disease beyond acute manifestations., Methods: Retrospective chart review of four patients with epilepsy, hippocampal sclerosis following viral encephalitis and NMDAR-antibodies in CSF., Results: The four patients were female, developed hippocampal sclerosis (in 3/4 in a step-wise progression) after Herpes simplex or Varicella zoster virus encephalitis and harboured immunoglobulin G antibodies against the NMDAR in their CSF. Two patients were treated with short-term immunosuppression but did not benefit., Conclusion: This case series presents the first tentative evidence in support of chronic autoimmune inflammation driving disease progression after viral encephalitis beyond the known acute immune-mediated relapses. The anecdotal nature of the data does not, however, permit conclusive judgement on causality. Should our findings be replicated in larger cohorts, the treatment of post-infectious epilepsy could potentially be expanded to include immunosuppressive strategies in antibody-positive cases., (Copyright © 2017 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.)

Herpes zoster is a reactivation of the latent varicella zoster virus. Among the complications of herpes zoster is zoster-associated limb paresis. The clinical and imaging features of patients with zoster-associated limb paresis due to plexopathies (zoster-associated plexopathy) have had limited description in the literature. The Mayo Clinic patient data base was searched by diagnostic code for patients diagnosed with herpes zoster between January 1, 1996, and September 30, 2012. Patients who met the inclusion criteria for zoster-associated limb paresis or herpes zoster with MRIs obtained were reviewed. Ten patients with zoster-associated plexopathy were identified. Imaging abnormalities were found in 70% of patients. Secondary denervation changes in shoulder girdle muscles and nerve T2 signal hyperintensity were the most frequent abnormalities (50%), followed by nerve enlargement (20%). Enhancement was not evident in any cases despite early imaging in 80% of the cohort. These results demonstrate the clinical utility of MR imaging in confirming the diagnosis of zoster-associated plexopathy., (© 2017 by American Journal of Neuroradiology.)

Competing Interests: The authors have completed and submitted the Methodist DeBakey Cardiovascular Journal Conflict of Interest Statement and none were reported.

Objective: The aim of this study was to report the case of a male patient with Parkinson disease who developed brachial plexopathy (BP) due to varicella-zoster virus, which was successfully treated with human immunoglobulin., Method: We report the case of a 75-year-old male subject with a diagnosis of Parkinson disease who came to our hospital complaining of pain, skin lesions, and strength loss in his right arm during the past 2 months. Physical examination revealed vesicular rash compatible with varicella-zoster virus lesions. Nerve conduction studies and magnetic resonance imaging of the brachial plexus showed inflammatory changes at that level. A trial with oral valacyclovir followed by intravenous methylprednisolone bolus was administered without further response. However, human intravenous immunoglobulin resulted in complete recovery of the symptoms., Conclusions: Human immunoglobulin is effective in BP due to zoster infection and must be considered if standard treatment fails. To the best of our knowledge, this is the first report of BP associated to zoster infection successfully treated with intravenous immunoglobulin.

We describe an extraordinary case of an immunocompetent patient who developed sacral-distribution zoster, followed 3months later by neurological disease that progressed for 6years and was attributed to varicella zoster virus (VZV) infection of the brain. Despite the prolonged infection, neurologic symptoms and signs resolved rapidly and completely after treatment with intravenous acyclovir., Competing Interests: statement All authors report no conflicts of interest., (Copyright © 2016 Elsevier B.V. All rights reserved.)

A wide range of infections (virus, bacteria, parasite and fungi) may cause cerebral vasculitides. Headache, seizures, encephalopathy and stroke are common forms of presentation. Infection and inflammation of intracranial vessels may cause pathological vascular remodelling, vascular occlusion and ischemia. Vasculitis in chronic meningitis may cause ischemic infarctions, and is associated with poor outcome. Appropriate neuroimaging (CT-angiography, MR-angiography, conventional 4-vessel angiography) and laboratory testing (specific antibodies in blood and CSF, CSF culture and microscopy) and even brain biopsy are needed to quickly establish the aetiology. Enhancement of contrast, wall thickening and lumen narrowing are radiological signs pointing to an infectious vasculitis origin. Although corticosteroids and prophylactic antiplatelet therapy have been used in infectious cerebral vasculitis, there are no randomized clinical trials that have evaluated their efficacy and safety. Stable mycotic aneurysms can be treated with specific antimicrobial therapy. Endovascular therapy and intracranial surgery are reserved for ruptured aneurysms or enlarging unruptured aneurysms.

Neurological complications of varicella-zoster virus (VZV) are infrequent and include various clinical pictures. The reactivation of VZV in patients with AIDS is generally associated with an acute and severe meningoencephalitis. We report the epidemiological, clinical and virological data from 11 consecutive patients with diagnosis of HIV/AIDS and central nervous system (CNS) involvement due to VZV. All patients were male and seropositive for HIV. The primary risk factor for HIV infection was unprotected sexual contact. The median of CD4 T cell count was 142 cells/µL. All of them presented signs and symptoms of meningoencephalitis. Six patients (54.5%) presented pleocytosis; they all showed high CSF protein concentrations with a median of 2.1 g/dL. Polymerase chain reaction of cerebrospinal fluid specimen was positive for VZV in all of them and they were treated with intravenous acyclovir at doses of 30/mg/kg/day for 21 days. Overall survival was 63% (7 of 11 patients). The four dead patients had low cellular counts in CSF, below the median of this parameter. VZV should be included among the opportunistic pathogens that can involve CNS with a diffuse and severe meningoencephalitis in patients with advanced HIV/AIDS disease.

Background: Varicella zoster virus (VZV) is known as one of the rare, but important, causes of both ischemic and hemorrhagic stroke. Most previously reported VZV-related hemorrhagic stroke and cerebral vasculitis are associated with anterior circulation because VZV spreads from trigeminal ganglia to the anterior circulation of Willis. The present study presents a patient with cerebellar hemorrhage, who was diagnosed with VZV encephalitis and vasculitis of the posterior inferior cerebellar artery., Case Report: A 75-year-old man with stupor was admitted to our hospital. Computed tomography revealed right intracerebellar hemorrhage, and magnetic resonance imaging revealed multiple high-intense signals throughout the brainstem and temporal lobe on fluid attenuation inversion recovery, suggestive of encephalitis. Cerebral angiography revealed stenosis of left posterior inferior cerebellar artery. Based on cerebrospinal fluid analysis, including anti-VZV IgG antibody and VZV DNA polymerase chain reaction, the patient was diagnosed with VZV encephalitis, vasculitis, and cerebellar hemorrhage., Conclusions: Both cerebral vasculitis and hemorrhagic stroke due to VZV can occur in the vertebrobasilar system. VZV may enter the central nervous system not only from trigeminal ganglia but also from other pathways. We should be aware that a VZV infection could cause cerebral vasculitis and hemorrhagic stroke in the vertebrobasilar system and in anterior circulation., (Copyright © 2015 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

A 73-year-old woman with a history of deceased donor kidney transplantation and a recent cytomegalovirus (CMV) infection, presented to the emergency department with an altered mental status. She was found to have varicella zoster virus VZV encephalitis based on cerebrospinal fluid analysis and was treated successfully with intravenous valaciclovir with an improvement in her mental status. A review of the literature shows very few case reports on patients with kidney transplantation developing VZV encephalitis. A few case reports and studies report an association between CMV and VZV infection. In these patients, CMV infection can cause a marked decline in immunity and this predisposes them to other infections. Such associations have also been reported between other types of virus infections from the Herpesviridae family. The risk of disseminated VZV infection increases in the presence of CMV infection., (2014 BMJ Publishing Group Ltd.)

Herpes zoster is reactivation of the varicella zoster virus that has remained dormant in the dorsal root ganglia since an earlier episode of chickenpox. Herpes zoster has variable clinical presentations, but meningo-encephalitis is not frequently encountered. There is growing evidence of both large and small vessel involvement in immunocompetent and immunocompromised patients, in contrast with the previous opinion that immunocompetent patients have vasculopathy in the large vessels while immunosuppressed patients have vasculopathy in the small vessels. We present the case of a patient in whom herpes zoster meningoencephalitis was complicated with multifocal vasculopathy with peripheral vascular disease; this is an unusual co-occurrence.

A 72-year-old man developed clinical features of giant cell arteritis (GCA) and ipsilateral ophthalmic-distribution zoster, followed within 2 weeks by VZV encephalitis and 2 months later by ischemic optic neuropathy. Temporal artery biopsy was histopathologically negative for GCA, but contained VZV antigen and VZV DNA in multiple non-contiguous (skip) areas. The collective clinical and laboratory findings revealed a remarkably close temporal association of zoster, multifocal VZV vasculopathy with temporal artery infection, biopsy-negative VZV-positive GCA and VZV encephalitis., (Copyright © 2014 Elsevier B.V. All rights reserved.)

This study explored the neurologic vascular complications of varicella zoster virus (VZV). We describe four patients presenting at our institution with neurologic involvement by VZV. MR and MRA studies of the intracranial arterial circulation in the head were read by board-certified radiologists using standard clinical procedures. On MRI, three patients had acute infarcts and in two instances irregularities and narrowings of vessels were visible. Many of these complications are recognized to be due to a vasculopathy affecting small or large vessels and resulting in cerebral infarctions and rarely hemorrhages. The pattern of cerebral infarction and vascular abnormalities is not specific and resembles those of vasculitis/vasculopathy from other causes. The central nervous system (CNS) vascular complications of VZV should be considered in the patients with simultaneous primary or prior VZV infection whose imaging studies show cerebral infarction and/or vasculitic appearing intracranial arteries.

Purpose of Review: Varicella zoster virus (VZV) reactivation results in zoster, which may be complicated by postherpetic neuralgia, myelitis, meningoencephalitis, and VZV vasculopathy. This review highlights the clinical features, laboratory abnormalities, imaging changes, and optimal treatment of each of those conditions. Because all of these neurological disorders produced by VZV reactivation can occur in the absence of rash, the virological tests proving that VZV caused disease are discussed., Recent Findings: After primary infection, VZV becomes latent in ganglionic neurons along the entire neuraxis. With a decline in VZV-specific cell-mediated immunity, VZV reactivates from ganglia and travels anterograde to the skin to cause zoster, which is often complicated by postherpetic neuralgia. VZV can also travel retrograde to produce meningoencephalitis, myelitis, and stroke. When these complications occur without rash, VZV-induced disease can be diagnosed by detection of VZV DNA or anti-VZV antibody in cerebrospinal fluid and treated with intravenous acyclovir., Summary: Awareness of the expanding spectrum of neurological complications caused by VZV reactivation with and without rash will improve diagnosis and treatment.

This is a case report of a 69-year-old morbidly obese woman who presented with mental status changes after she was treated with acyclovir for shingles. The predominant symptoms were word-finding difficulties and visual hallucinations. Complicating her presentation was acyclovir-induced acute renal injury causing her creatinine level to rise up to 7.4 mg/dL. Acyclovir was discontinued on the suspicion of acyclovir neurotoxicity. Even though PCR for varicella zoster virus in the cerebrospinal fluid was positive, acyclovir was not restarted and the patient continued to improve and returned to her baseline.