VZV infections …

Amanda L Piquet MD

Infectious Disorders

Updated 05.30.2024
Released 08.19.1997
Expires For CME 05.30.2027

Varicella-zoster virus infections of the nervous system

Author: Amanda L Piquet MD

See Contributor Disclosures

Editor: John E Greenlee MD

Varicella-zoster virus infections of the nervous system

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Introduction

Overview

Varicella-zoster virus causes chickenpox (varicella) during primary infection, often in childhood. The virus becomes latent in dorsal root ganglia and can reactivate years later to produce shingles (zoster, zona) in adults, as well as postherpetic neuralgia and vasculopathies, which may involve brain, spinal cord, cranial nerves, or peripheral nerves or plexus. Diagnosis of varicella-zoster virus infection of the central and peripheral nervous system is critical as antiviral therapy can suppress productive infection with clinical benefit.

Key points

	• Varicella-zoster virus central nervous system infection can have various presentations, including encephalitis, meningitis, cranial neuropathies, vasculopathy, and myelitis.
	• Varicella-zoster virus has been identified as accounting for 15% to 23% of viral encephalitis in the United States (79).
	• The absence of a rash or history of shingles does not exclude the possibility of varicella-zoster virus meningoencephalitis, myelopathy, or vasculopathy (29; 72).
	• Identifying varicella-zoster virus as the etiology of CNS involvement can be challenging especially in the setting of no preceding rash. However, a rapid and accurate diagnosis is paramount as early initiation of antivirals is likely to improve patient outcomes.

Historical note and terminology

Varicella-zoster virus causes chickenpox (varicella) as a primary infection in childhood or, more rarely, in adults. The virus then becomes latent in neurons of dorsal root ganglia, cranial nerve ganglia, and autonomic ganglia. Varicella-zoster virus can reactivate years later to produce shingles (zoster) in adults. Chickenpox is a generalized exanthem, whereas shingles is usually limited to one or more adjacent sensory dermatomes. However, in immunocompromised individuals, systemic involvement can be seen in the setting of reactivation. Herpes zoster was described in medieval literature, and it was recognized as caused by varicella-zoster virus by the end of the 19th century (89). The relationship between varicella and zoster was not recognized until the end of the 19th century partially because varicella was not differentiated from variola (smallpox) (69). In 1888 Von Bokay suggested that chickenpox and shingles were related after observing that susceptible children could acquire chickenpox after exposure to adults with shingles (85). Varicella was shown to be infectious in 1875 by Steiner, and shingles in 1925 by Kundratitz (81; 48). The characteristic intranuclear inclusion bodies seen in varicella-zoster virus infections were described in chickenpox lesions by Tyzzer in 1906 and in shingles lesions by Lipschultz in 1921 (84; 54). In 1943 Garland suggested that shingles was due to the reactivation of latent varicella-zoster virus (25). The tissue culture and serologic studies of Weller and colleagues firmly established that chickenpox and shingles were due to a single etiologic agent (89; 90).

Developments include the use of polymerase chain reaction and in situ hybridization techniques to demonstrate that varicella-zoster virus DNA is latently present in trigeminal and thoracic ganglia (56). Specific prophylactic and therapeutic agents have also become available. Intravenous acyclovir is the mainstay of treatment for varicella-zoster virus dissemination and neurologic complications. Although not indicated for neurologic involvement, varicella-zoster virus immune globulin can prevent varicella infection in exposed seronegative pregnant women and immunocompromised children and newborns (05). A report of two neonates with severe varicella, despite intravenous immunoglobulin, suggests that infected infants should also receive acyclovir (75). In 1995 the U.S. Food and Drug Administration approved a live attenuated varicella-zoster virus vaccine (Varivax-Merck); this vaccine has been recommended for people 12 months of age or older, who are in good health and without a history of prior varicella-zoster virus infection (05).

Clinical manifestations

Presentation and course

The clinical manifestations of varicella-zoster virus infections can be divided into primary varicella zoster infection (chickenpox) and reactivated varicella-zoster virus infection (dermatomal shingles or disseminated herpes zoster). Varicella-zoster virus is a neurotropic human herpesvirus, and the cause of neurologic complications has been postulated as either direct viral invasion through retrograde infection of neurons or immune-mediated mechanisms (71; 59). In the setting of virus reactivation, varicella-zoster virus vasculopathy can occur as an uncommon but life-threatening neurologic complication for which clinical presentations will be discussed in more detail. Studies with Gilden and colleagues have identified the presence of varicella-zoster virus antigen in the adventitia of vessels walls, thus, supporting the mechanism of varicella-zoster virus spreading transaxonally from ganglionic afferent fibers to the artery (64). Pathologically, three main patterns have been described including large and small vessel vasculopathies and, rarely, ventriculitis (64). Clinically, patients can present with various manifestations, including encephalopathy, stroke, seizures, myelitis, cranial neuropathies, and even temporal arteritis.

In this section, both primary varicella-zoster virus and complications of virus reactivation will be discussed in detail as well as potential neurologic complications.

Acute primary varicella infection (chickenpox). Chickenpox is an exanthematous illness that occurs with primary varicella-zoster virus infection. The rash typically starts on the scalp and then spreads to the trunk. The distal extremities are usually involved to a lesser extent. Lesions of different ages are seen. Early lesions are rose-colored macules with clear vesicles in the center. Within hours, the vesicles become purulent and, later, dry and crusted. A prodromal syndrome of 1 to 2 days of fever and malaise is more likely to be seen in adults. During the exanthem, fever usually lasts for 2 to 3 days. Non-neurologic complications, such as varicella-zoster virus pneumonitis and secondary bacterial infections (58) can be seen; however, these complications are more common in adults compared to children. In some patients, the infection can be slight, with only rare skin lesions. Reye syndrome (nausea, vomiting, headache, and encephalopathy with progression to coma) historically has been seen in the setting of primary varicella infection; however, since the discontinuation of salicylate use in children, this complication is almost nonexistent (71).

Zoster or varicella-zoster virus reactivation. Herpes zoster can occur anywhere in the neuraxis, but it is most common in the thoracic region. The second most common involved area is the ophthalmic division of the trigeminal nerve; this can lead to ocular involvement and blindness. Herpes zoster is not only more common in immunocompromised patients, but it is also more likely in these patients to become generalized, with diffuse cutaneous lesions and internal organ involvement. In a study of 282 patients with varicella-zoster virus reactivation who were hospitalized in the department of neurology, the most common clinical manifestations were trigeminal nerve ganglionitis with rash, dorsal root ganglionitis with rash (most commonly in thoracic region), CNS infection (eg, encephalitis, meningitis, or myelitis), facial nerve palsy, and less commonly dorsal root ganglionitis with radiculitis (80). The age distribution in this cohort showed a sharp rise in incidence after the age of 50 years and peaking in the eighth decade of life (80).

Postherpetic neuralgia. Postherpetic neuralgia is persistence of the pain of herpes zoster for more than 4 to 6 weeks after the rash disappears and can persist for months to years (57). It is estimated that 5% to 20% of patients with zoster will develop postherpetic neuralgia (47); the risk increases in patients over the age of 60 years and cases with ophthalmic involvement (24).

Neurologic complications of varicella-zoster virus. Varicella-zoster virus is known to cause neurologic involvement; however, complications following primary infections are rare. The main neurologic syndromes related to primary acute varicella infections are acute cerebellar ataxia, meningitis, encephalitis, and myelitis; however, varicella-zoster virus can involve every level of the neurologic system, and prognosis appears to differ between different levels of involvement. In a retrospective review of 72 patients with confirmed varicella-zoster virus positivity by PCR in the cerebrospinal fluid, aseptic meningitis had a good prognosis, whereas the presence of encephalitis, myelitis, and stroke have a higher risk of mortality, peripheral involvement, and a long-term sequelae (49). Neurologic complications occur in approximately 1 in 2000 cases of varicella among children (74).

Acute cerebellar ataxia. Acute cerebellar ataxia is the most common extracutaneous complication of chickenpox in healthy children. It can precede the exanthema or, in rare cases, occur in the absence of an exanthema, but usually occurs 5 to 10 days after the rash (77; 19). Although most commonly seen as a neurologic complication of varicella-zoster virus infection in healthy children, it can be a rare manifestation of viral reactivation in adults (19). It usually presents with truncal ataxia and tremor. MRI findings can include bilateral and symmetric T2 hyperintense changes in the cerebellar cortex with or without associated contrast enhancement (93). Cerebrospinal fluid studies typically demonstrate a pleocytosis.

This illness is typically self-limiting, and generally there is complete recovery. Treatment remains unclear, but experts typically recommend IV acyclovir, which likely hastens recovery and reduces morbidity. That said, varicella-zoster virus cerebellitis is often self-limited, and patients typically recover within weeks without long-term sequalae (19). The pathophysiologic mechanism of cerebellar ataxia from varicella-zoster virus remains elusive with hypothesis including direct infection versus postinfectious, autoimmune mechanisms.

Meningitis or encephalitis. Both viral meningitis and encephalitis can be seen with primary varicella-zoster virus infection; furthermore, encephalitis is often severe, and most cases occur within weeks following the exanthema. In fact, varicella-zoster virus is likely the second most common pathogen causing severe sporadic viral encephalitis after herpes simplex infection (79). Many patients will present primarily with confusion and seizures. MRI is almost always abnormal, and findings can include ischemic or hemorrhagic changes. Cerebrospinal fluid studies typically demonstrate a pleocytosis and elevated protein.

Pathological studies have shown that many cases of encephalitis are due to either large or small vessel vasculopathy as a result of the viral infection of the vascular endothelium (22) rather than direct invasion of the brain parenchyma. Kleinschmidt-DeMasters and colleagues also mention involvement of oligodendrocytes to cause demyelination (45). In fact, the small vessel vasculopathy that leads to leukoencephalopathy was first described by Horten and colleagues and later confirmed by Morgello and colleagues (40; 62). Both demyelination and necrosis can be seen in the small vessel disease of varicella-zoster virus encephalitis (40; 62; 37; 04). This also supports that zoster reactivation can present as a post-infectious, immune-mediated demyelinating process typically seen in acute disseminated encephalomyelitis. Acute disseminated encephalomyelitis typically presents as encephalitis with progressive altered mental status, confusion, headache, and fever. MRI classically demonstrates multiple deep and subcortical white matter abnormalities, typically with gadolinium enhancement consistent with demyelination.

Myelitis. Varicella-zoster virus myelitis is less common than encephalitis. In the study of 282 patients with varicella-zoster virus reactivation admitted to the neurology service, 34 patients had CNS infection, in which eight patients (53%) had encephalitis, 15 (44%) had meningitis, and one patient (3%) had myelitis (80). Most cases of myelitis have a radiographical appearance and clinical presentation of typical transverse myelitis. The myelopathy characteristically presents with upper motor neuron signs, including weakness, hyperreflexia, and positive Babinski sign. Myelitis can be a complication of primary varicella-zoster virus infection or reactivation and can occur with or without the classical zoster rash. Although myelitis has typically been described in immunocompromised patients, it has also occurred in immunocompetent patients (31). MRI will typically show a longitudinally extensive lesion, likely with enhancement. The pathogenesis is likely similar to that of encephalitis with small vessel vasculopathy with or without demyelination and necrosis. Additionally, varicella-zoster virus vasculopathy has been reported in spinal cord infarction (31). If myelopathy is from infarction, diffusion-restriction abnormalities may be seen in the cord.

Cranial neuropathies. Varicella-zoster virus is latent in cranial nerve ganglia; therefore, multiple cranial nerve palsies can develop typically days to weeks after zoster (29). Involvement of these nerves can result in debilitating weakness and pain. Several classic syndromes have been described. Herpes zoster ophthalmicus refers to reactivation in the V1 trigeminal nerve dermatome and can lead to multiple complications, including cranial neuropathies, retinal necrosis, uveitis and scleritis, and even contralateral ischemic or hemorrhagic strokes (60). Ophthalmoplegia is a well-documented complication with involvement of cranial nerve 3, 4, or 6 or any combination of these. Optic neuritis has been reported in the immunocompromised as well as the immunocompetent and, even more rarely, after varicella-zoster virus vaccination (07; 39). Ramsay Hunt syndrome type 2 is caused by varicella-zoster virus of the geniculate ganglion and includes the combination of peripheral facial palsy and ipsilateral external auditory canal (zoster oticus) involvement. Patients commonly present with tinnitus, severe ear pain, hearing loss, vertigo, or nystagmus. Importantly, varicella-zoster virus associated polyradiculoneuritis (18) and polyneuritis cranialis (63; 30) have been reported in the absence of rash.

Arteritis. Varicella-zoster virus vasculopathy can manifest as a stroke, aneurysm, dissection, or other vascular abnormalities. Presentations can be acute and monophasic or chronic and progressive. Given varicella-zoster virus’ tropism for vessels, it can cause isolated ischemic and hemorrhagic infarcts (03) and the development of multiple cerebral aneurysms (53), and more recent evidence has suggested infection may lead to temporal arteritis or giant cell arteritis (68). Giant cell arteritis is typically seen in individuals over the age of 50 years, and diagnosis is made by clinical features including headaches, acute onset visual changes, jaw claudication, accompanying symptoms of polymyalgia rheumatic, and suggestive laboratory values including a high erythrocyte sedimentation rate (ESR). Diagnosis is confirmed with temporal artery biopsy. Studies have found varicella-zoster virus in the temporal arteries of some patients with signs and symptoms of giant cell arteritis, including patients found to be giant cell arteritis biopsy-positive as well as -negative (27). The mainstay treatment for giant cell arteritis is prolonged corticosteroids, but given these studies, the use of antiviral in addition to steroids has been suggested (30).

Rare cases of dissection resulting from varicella-zoster virus vasculopathy have been described (68). Two pediatric cases had a rash followed by carotid dissections in the setting of vigorous activity 2 to 4 weeks later (17).

A study of 20 varicella-zoster virus vasculopathy cases demonstrated 63% had rash, 67% had a CSF pleocytosis, 97% had braining imaging abnormalities, and 70% had angiographic abnormalities (67).

Acute inflammatory demyelinating polyradiculoneuropathy or Guillain-Barre syndrome. Acute inflammatory demyelinating polyradiculoneuropathy or Guillain-Barre syndrome has been identified as a rare complication of herpes zoster. A study done with data from a Taiwan health registry found that although GBS was a rare complication, the risk of GBS 2 months after herpes zoster was significantly higher compared to age- and sex-matched controls (44). Clinical features of GBS included progressive, symmetric muscle weakness and loss of deep-tendon reflexes over days to a week after symptom onset. Presentation severity can vary leading to weakness of respiratory, facial, and bulbar muscles.

Autonomic and gastrointestinal involvement. Varicella-zoster virus can infect and become latent in sensory, enteric, and other autonomic neurons. Reactivation in enteric neurons can cause a painful gastrointestinal disorder (“enteric zoster”) without cutaneous manifestation (26). Varicella-zoster virus has been identified to establish latency in autonomic ganglia as well (33).

Dementia (chronic sequelae). Studies have suggested that herpes simplex virus and/or varicella zoster infection are associated with an increased risk of dementia (78). A study conducted in Taiwan based on the National Health Insurance Research Database claimed that varicella-zoster virus was associated with an increased risk of dementia (HR = 1.11) (15), and a cohort study conducted in South Korea revealed that patients with varicella-zoster virus had a higher risk of dementia (adjusted HR = 1.12) (08). However, other studies report contradictory results with no association of varicella and dementia seen in the United Kingdom (87) or with the national Danish data (42). At this point data remain conflicting, and the link between varicella zoster virus and dementia remains unclear. From a pathological standpoint, some data have suggested that varicella infection may increase the toxic amyloid burden, thus contributing to amyloid-associated disease progression as a possible link (12).

Prognosis and complications

Childhood chickenpox tends to be a benign, self-limited disease, and overall prognosis is good in immunocompetent children. However, in adolescent, adult, and immunocompromised individuals, the disease can be much more severe. Prior to the introduction to the varicella vaccine, acute complications were more prevalent; those primarily include secondary bacterial infections of skin and soft tissue, pneumonia, and hepatitis. The major complications of varicella-zoster virus infection are the generalized and reactivated infection, which are typically more severe in immunocompromised individuals. Postherpetic neuralgia can last for years or even decades and can be a significant source of morbidity. The prognosis for arteritis often depends on the extent of the neurologic involvement and underlying immunocompromising illness.

Clinical vignette

This is a case of a 32-year-old Brazilian male who moved to the United States about 8 years prior to presentation. He was diagnosed with HIV 6 years before he presented to the emergency department with fever, chills, headache, and right-sided face, eye, and jaw pain. He endorsed severe neck pain over the past week and dysphagia for 4 days. In terms of his HIV, he was anti-retroviral naïve, and his most recent CD4 count was 208 cells/mm3. When he arrived at the emergency department, he was febrile with a temperature of 102 degrees Fahrenheit. His physical examination was remarkable for multiple, small vesicular lesions on his face, neck, and chest. Due to poor mental status and respiratory distress, he was intubated shortly after his arrival. Off sedation he would open his eyes to voice and followed simple commands. Both pupils were reactive to light with asymmetry; left pupil was 6 to 4 mm, and his right pupil was 8 to 6 mm. His face was symmetric, and he moved all four extremities spontaneously and symmetrically. His reflexes were brisk throughout, and he had bilateral positive Babinski sign.

He had a non-contrast head CT that showed no evidence of hemorrhage, herniation, or mass effect, so a lumbar puncture was obtained. His CSF analysis demonstrated 1850 white blood cells (9% neutrophils, 68% lymphocytes, 19% monocytes), 805 red blood cells, total protein 337, and glucose 132 (with a serum glucose of 180). Negative infectious studies on the CSF included a Gram stain and culture with acid fast bacillus (AFB) stain and culture, herpes simplex virus (HSV) polymerase chain reaction (PCR), enterovirus PCR, cytomegalovirus (CMV) PCR, human herpes virus 6 (HHV-6) PCR, Epstein-Barr virus (EBV) PCR, West Nile IgG/IgM, and cryptococcal antigen. His varicella-zoster virus PCR was positive in the CSF. Varicella-zoster virus IgM and IgG were not tested in the CSF.

Varicella-zoster virus in adult male (MRI)

(A) Fluid attenuated inversion recovery (FLAIR) signal abnormalities are seen throughout the posterior circulation region including the cerebellum and medulla (see white thin arrows) with associated restricted diffusion changes (n...

This patient was diagnosed with varicella-zoster virus meningoencephalitis and disseminated varicella-zoster virus infection in the setting of an immunocompromised state with HIV. He was started on intravenous acyclovir as well as meningitic dosing of vancomycin, ceftriaxone, and ampicillin until his CSF culture were negative for bacterial infection for 48 hours. Acyclovir was continued with dosing of 10 mg/kg every 8 hours for a total of 14 days. He was also started on antiretroviral therapy.

This case highlights the severity of varicella-zoster virus meningoencephalitis in an immunocompromised patient as his course was complicated by disseminated disease and vesicular eruption involving his face, neck, and chest. The classical appearance of the rash facilitated a rapid diagnosis in this case. He presented with typical findings of meningoencephalitis, including fever, nuchal rigidity, headache, and confusion. CSF studies were consistent with an infectious etiology and confirmed the diagnosis with varicella-zoster virus PCR positivity. Varicella-zoster virus antibodies in the CSF were not tested in this case; however, these would have been imperative to check in the setting of a negative PCR. Varicella-zoster virus PCR in the CSF have a sensitivity of 80% and specificity of 98% in patients with HIV, whereas varicella-zoster virus antibodies have a higher sensitivity (22). MRI findings show classical findings of varicella-zoster virus encephalitis, including ischemic changes and brainstem and cerebellar involvement.

Biological basis

Etiology and pathogenesis

Chickenpox and herpes zoster are due, respectively, to primary and reactivated infection by varicella-zoster virus, a human herpes virus.

In the animal model of varicella, varicella-zoster virus invades through the mucosa of the upper respiratory tract and oropharynx and possibly the conjunctiva. Initially, replication occurs at these primary inoculation sites in the head and neck. After an interval of 4 to 5 days, primary viremia occurs and disseminates the virus throughout the body. A week later, after replication in secondary sites (reticuloendothelial system cells), a second viremia leads to the exanthem. The total incubation period is usually 14 to 15 days, with a range of 10 to 20 days (91).

After primary varicella-zoster virus infection, the virus becomes latent in the sensory root ganglia. As immunity, particularly cellular immunity, wanes with age or disease, the virus reactivates, replicates in the dorsal root ganglia, and may travel down the sensory nerve to infect the skin in the dermatome innervated by the nerve, resulting in herpes zoster (64). In acute zoster, a hemorrhagic inflammation involving the dorsal root ganglia and nerve can be seen. In patients with postherpetic neuralgia, fibrosis and cell loss in the dorsal root ganglion with loss of myelin occur (88). Occasionally, the immune response is able to abort the cutaneous lesions but not the dorsal root ganglia virus replication with subsequent inflammation, necrosis, and fibrosis of the ganglia. In this setting, the patient may present with radicular pain without the skin lesions (zoster sine herpete) (35). Varicella-zoster virus DNA has also been detected in human nodose and celiac ganglion of the autonomic nervous system (33).

Varicella-zoster virus has been detected in the involved blood vessels, specifically in the setting of vasculopathy, this develops after the virus reactivates from ganglia and spreads transaxonally to arterial adventitia resulting in persistent inflammation (43).

Reactivation of varicella-zoster virus can also result in generalized infection, particularly in immunocompromised patients, presumably through a hematogenous route. This can result in granulomatous arteritis, which may lead to stroke, myelitis, meningitis, and encephalitis (29; 03).

Prevention

There are now vaccines for varicella (Varivax^®, Merck) and zoster (Zostavax^®, Merck; and SHINGRIX, GlaxoSmithKlein). The World Health Organization currently recommends that varicella vaccination be implemented in all countries where varicella is an important public health concern but only if resources allow for sustained vaccination rates of more than 80% as lower rates may be associated with increased morbidity and mortality among vulnerable populations (06).

A 2-dose immunization schedule for varicella vaccine has decreased the incidence of breakthrough varicella and is now recommended (02). Children should receive the first dose at 12 to 15 months and the second dose at 4 to 6 years old.

Varicella vaccine given to children within 3 days of varicella-zoster virus exposure may reduce the rate and severity of infection (55).

The lifetime risk of varicella-zoster virus reactivation is around 30% (86). Therefore, safe and effective vaccination has the potential to reduce the burden of varicella-zoster virus disease. Vaccination against varicella-zoster virus (Zostavax, a live vaccination) given to adults 60 years old and older resulted in decreased morbidity from herpes zoster and postherpetic neuralgia (70). In October 2017, a recombinant, adjuvanted zoster vaccine (Shingrix) was approved for the prevention of herpes zoster in adults over 50 years of age with recommended use in immunocompetent adults (23). The Shingrix vaccine has been shown to reduce varicella-zoster virus reactivation by more than 95% and, thus, has largely supplanted the live attenuated vaccine in the U.S. due to improved efficacy and safety (13). As of 2021, Shringrix has also received full FDA approval in the U.S. for administration for immunocompromised patients over the age of 18 years old (it was previously only approved for those over 50 years old).

As Shingrix is a non-live vaccine, it is considered safe in the immunocompromised population. There are two studies demonstrating the prevention of herpes zoster in autologous hematopoietic stem cell transplant recipients and those with hematological malignancies (20; 21).

For immunocompromised patients at risk for primary infection after varicella-zoster virus exposure, varicella-zoster virus immune globulin is recommended. Varicella-zoster virus immune globulin administration is also recommended for susceptible pregnant women but does not protect the fetus from sequelae (05). Varicella vaccine is not recommended for pregnant women (02). Herpes zoster, meningitis, and encephalitis due to the varicella-zoster virus strain in the varicella vaccine have been reported (52; 41; 16). CNS vasculopathy due to vaccine varicella-zoster virus strain has been reported in patients with DOCK8 deficiency (76).

Diagnostic workup

The diagnosis of chickenpox and herpes zoster is primarily clinical. Tzanck smears of the skin lesions may demonstrate intranuclear inclusions. Virus from vesicles can be isolated in cell culture. PCR testing of skin vesicle fluid in chickenpox and herpes zoster may identify varicella-zoster virus. Diagnosis of vaccine-modified varicella is challenging, and PCR testing of the macular or popular lesions often seen can confirm diagnosis (50). Antibody titers rise after primary varicella-zoster virus infection and can be used to confirm diagnosis retrospectively. Patients with zoster or immune deficiency may not demonstrate a rise in antibodies.

In varicella-zoster virus encephalitis, brain imaging may show large and small ischemic or hemorrhagic infarcts, often both. Deep-seated ischemic or demyelinating white matter lesions often predominate (04). The EEG shows nonspecific slowing. Varicella-zoster virus is almost never isolated from CSF by culture, but CSF can be examined by PCR for detection of varicella-zoster virus DNA (46). CSF antibodies to the varicella-zoster virus may also be found in varicella-zoster virus infections of the nervous system and in the setting of vasculopathy, particularly more chronic presentations, are more sensitive than PCR in varicella-zoster virus vasculopathy (66). For more acute, encephalitic clinical pictures, DNA PCR testing is often sufficient. However, if CNS disease is suspected, CSF should be examined for both varicella-zoster virus DNA by PCR and varicella-zoster virus–specific antibody. There are newer meningitis Biofire FilmArrays© available that allow for broad infectious testing with a multiplex PCR, thus, allowing the ability to simultaneously test for several infectious agents. These methodologies appear to have acceptable-to-high sensitivities for identifying bacteria and some viruses, however not all of them. For varicella-zoster virus specifically, sensitivities for PCR were between 75.5% and 93.8%, and, importantly, antibody testing is not included (82). When there is clinical suspicion for varicella-zoster virus, it is best to still relay on the standard CSF varicella-zoster virus DNA by PCR and varicella-zoster virus–specific antibody. Pathologic specimens may show classic Cowdry A inclusion bodies and can be tested for varicella-zoster virus by in situ hybridization and PCR.

Management

Childhood chickenpox tends to be a benign, self-limited disease. Primary or secondary varicella-zoster virus infection in immunocompromised individuals can be treated with acyclovir. Resistance can be a problem in individual patients, and foscarnet has been used to treat acyclovir-resistant varicella-zoster virus infections (36).

Varicella-zoster virus encephalitis, myelitis, and vasculopathy are treated with intravenous acyclovir. Gilden and colleagues suggest that patients with varicella-zoster virus vasculopathy be treated with 10 to 15 mg/kg of intravenous acyclovir every 8 hours for 7 to 10 days. Steroid therapy (prednisone 60 to 80 mg/day for 3 to 5 days) should be considered as well, in conjunction with acyclovir. Concomitant or delayed administration of corticosteroids may help mitigate the strong inflammatory cascade and immune response seen with the varicella-zoster virus infection; however, there are no randomized clinical trials available, and expert opinion is largely based on case reports and case series (65; 28). Immunocompromised patients may require longer treatment. Repeat CSF should be negative for varicella-zoster virus by PCR prior to discontinuing antiviral treatment (32). As varicella-zoster virus antigen is frequently found in temporal artery biopsies of patients with giant cell arteritis, consideration of the addition of antiviral therapy to corticosteroids for treatment of temporal arteritis has been suggested (34).

Famciclovir, used in the acute phase of herpes zoster, has been shown to reduce the duration of postherpetic neuralgia in patients older than 50 years of age who have a severe rash (83). Valacyclovir has also been shown to shorten the duration of postherpetic neuralgia in patients older than 50 years of age (10). Either valacyclovir or famciclovir is the preferred drug of choice over acyclovir for zoster due to less frequent dosing. As prompt antiviral therapy may not only shorten the acute phase of herpes zoster but also lessen the duration and severity of postherpetic neuralgia, prompt diagnosis and treatment are critical. Optimal duration of treatment is not clear.

The treatment of established postherpetic pain is often difficult. Recommended first-line therapies include tricyclic antidepressants (amitriptyline, nortriptyline, or desipramine), gabapentin and pregabalin, or topical lidocaine patches and second-line therapies with oral opioid therapy and topical capsaicin cream (57). Despite these therapies, postherpetic neuralgia pain can be intractable.

References

01: Ahn KH, Park YJ, Hong SC, et al. Congenital varicella syndrome: a systematic review. J Obstet Gynaecol 2016;36(5):563-6. PMID 26965725
02: American Academy of Pediatrics Committee on Infectious Diseases. Prevention of varicella: recommendations for use of varicella vaccines in children, including a recommendation for a routine 2-dose varicella immunization schedule. Pediatrics 2007;120(1):221-31. PMID 17606582
03: Amlie-Lefond C, Gilden D. Varicella zoster virus: a common cause of stroke in children and adults. J Stroke Cerebrovasc Dis 2016;25(7):1561-9. PMID 27138380
04: Amlie-Lefond C, Kleinschmidt-DeMasters BK, Mahalingam R, Davis LE, Gilden DH. The vasculopathy of varicella-zoster encephalitis. Ann Neurol 1995;37:784-90. PMID 7778852
05: Anonymous. Prevention of varicella: recommendations of the advisory committee on immunization practices (ACIP). Centers for Disease Control. MMWR Recomm Rep 1996;45(RR-11):1-36. PMID 8668119
06: Anonymous. Varicella and herpes zoster vaccines: WHO position paper, June 2014--recommendations. Vaccine 2016;34(2):198-9. PMID 26723191
07: Azevedo AR, Simões R, Silva F, et al. Optic neuritis in an adult patient with chickenpox. Case Rep Ophthalmol Med 2012;2012:371584. PMID 23320222
08: Bae S, Yun SC, Kim MC, et al. Association of herpes zoster with dementia and effect of antiviral therapy on dementia: a population-based cohort study. Eur Arch Psychiatry Clin Neurosci 2021;271(5):987-97. PMID 32613564
09: Benoit G, Etchemendigaray C, Nguyen-Xuan HT, Vauloup-Fellous C, Ayoubi JM, Picone O. Management of varicella-zoster virus primary infection during pregnancy: a national survey of practice. J Clin Virol 2015;72:4-10. PMID 26356985
10: Beutner KR, Friedman DJ, Forszpaniak C, Anderson PL, Wood MJ. Valacyclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother 1995;39:1546-53. PMID 7492102
11: Brunell PA, Kotchmar GS. Zoster in infancy: failure to maintain virus latency following intrauterine infection. J Pediatr 1981;98:71-3. PMID 7452407
12: Bubak AN, Como CN, Coughlan CM, et al. Varicella-Zoster virus infection of primary human spinal astrocytes produces intracellular amylin, amyloid-β, and an amyloidogenic extracellular environment. J Infect Dis 2020;221(7):1088-97. PMID 31665341
13: Centers for Disease Control and Prevention. Protect your patients with the shingles vaccine. Available at: cdc.gov/vaccines/hcp/vis/vis-statements/shingles-recombinant.html. Accessed February 2023.
14: Centers for Disease Control and Prevention. Shingles (Herpes Zoster). cdc.gov/shingles/hcp/clinical-overview.html. Accessed January 2017.
15: Chen VC, Wu SI, Huang KY, et al. Herpes zoster and dementia: a nationwide population-based cohort study. J Clin Psychiatry 2018;79(1):16m11312. PMID 29244265
16: Chouliaras G, Spoulou V, Quinlivan M, Breuer J, Theodoridou M. Vaccine-associated herpes zoster ophthalmicus and encephalitis in an immunocompetent child. Pediatrics 2010;125(4):e969-72. PMID 20194287
17: Constantinescu CS. Association of varicella-zoster virus with cervical artery dissection in 2 cases. Arch Neurol 2000;57:427. PMID 10714677
18: Cortese A, Tavazzi E, Delbue S, et al. Varicella zoster virus-associated polyradiculoneuritis. Neurology 2009;73:1334-5. PMID 19841388
19: Cross CP, English SW, Krause MA, Zalewski NL. Acute truncal ataxia in a healthy adult with varicella zoster virus cerebellitis: A case report and literature review. J Neurol Sci 2019;400:186-7. PMID 30981122
20: Curran D, Matthews S, Rowley SD, et al. Recombinant zoster vaccine significantly reduces the impact on quality of life caused by herpes zoster in adult autologous hematopoietic stem cell transplant recipients: a randomized placebo-controlled trial (ZOE-HSCT). Biol Blood Marrow Transplant 2019;25(12):2474-81. PMID 31394276
21: Dagnew AF, Ilhan O, Lee WS, et al. Immunogenicity and safety of the adjuvanted recombinant zoster vaccine in adults with haematological malignancies: a phase 3, randomised, clinical trial and post-hoc efficacy analysis. Lancet Infect Dis 2019;19(9):988-1000. PMID 31399377
22: Debiasi RL, Tyler KL. Molecular methods for diagnosis of viral encephalitis. Clin Microbiol Rev 2004;17(4):903-25. PMID 15489354
23: Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep 2018;67(3):103-8. PMID 29370152
24: Forbes HJ, Thomas SL, Smeeth L, et al. A systematic review and meta-analysis of risk factors for postherpetic neuralgia. Pain 2016;157(1):30-54. PMID 26218719
25: Garland J. Varicella following exposure to herpes zoster. N Engl J Med 1943;228:336-7.
26: Gershon M, Gershon A. Varicella-zoster virus and the enteric nervous system. J Infect Dis 2018;218(suppl_2):S113-9. PMID 30247599
27: Gilden D. Association of varicella zoster virus with giant cell arteritis. Monoclon Antib Immunodiagn Immunother 2014;33(3):168-72. PMID 24893151
28: Gilden D, Cohrs RJ, Mahalingam R, Nagel MA. Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment. Lancet Neurol 2009a;8(8):731-40. PMID 19608099
29: Gilden D, Nagel M, Cohrs R, Mahalingam R, Baird N. Varicella zoster virus in the nervous system. F1000Res 2015a;4. PMID 26918131
30: Gilden D, Nagel MA. Varicella zoster virus and giant cell arteritis. Curr Opin Infect Dis 2016;29(3):275-9. PMID 26871403
31: Gilden D, Nagel MA, Ransohoff RM, Cohrs RJ, Mahalingam R, Tanabe JL. Recurrent varicella zoster virus myelopathy. J Neurol Sci 2009b;276:196-8. PMID 18945446
32: Gilden DH. Varicella zoster virus and central nervous system syndromes. Herpes 2004;11(Suppl 2):89A-94A. PMID 15319095
33: Gilden DH, Gesser R, Smith J, et al. Presence of varicella-zoster virus and HSV-1 DNA in human nodose and celiac ganglia. Virus genes 2001;23(2):145-7. PMID 11724266
34: Gilden DH, White T, Khmeleva N, al. Prevalence and distribution of varicella-zoster virus in temporal arteries of patients with giant cell arteritis. Neurology 2015b;84(19):1948-55.** PMID 25695965
35: Gilden DH, Wright RR, Schneck SA, Gwaltney JM, Mahalingam R. Zoster sine herpete, a clinical variant. Ann Neurol 1994b;35:530-3. PMID 8179298
36: Gnann JW. Antiviral therapy of varicella-zoster virus infections. In: Arvin A, Campadelli-Fiume G, Mocarski E, et al, editors. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press, 2007:Chapter 65. PMID 21348091
37: Gray F, Belec L, Lescs MC, et al. Varicella-zoster virus infection of the central nervous system in the acquired immune deficiency syndrome. Brain 1994;117(Pt 5):987-99. PMID 7953606
38: Hales CM, Harpaz R, Joesoef MR, Bialek SR. Examination of links between herpes zoster incidence and childhood varicella vaccination. Ann Int Med 2013;159(11):739-45. PMID 24297190
39: Han SB, Hwang JM, Kim JS, Yang HK. Optic neuritis following varicella zoster vaccination: report of two cases. Vaccine 2014;32(39):4881-4. PMID 25045807
40: Horten B, Price RW, Jimenez D. Multifocal varicella-zoster virus leukoencephalitis temporally remote from herpes zoster. Ann Neurol 1981;9:251-66. PMID 6261672
41: Iyer S, Mittal MK, Hodinka RL. Herpes zoster and meningitis resulting from reactivation of varicella vaccine virus in an immunocompetent child. Ann Emerg Med 2009;53(6):792-5. PMID 19028409
42: Johannesdottir Schmidt SA, Veres K, Sørensen HT, Obel N, Henderson VW. Incident herpes zoster and risk of dementia: a Population-based Danish cohort study. Neurology 2022;99(7):e660-8. PMID 35676090
43: Jones D, Blackmon A, Neff CP, et al. Varicella-zoster virus downregulates programmed death ligand 1 and major histocompatibility complex class I in human brain vascular adventitial fibroblasts, perineurial cells, and lung fibroblasts. J Virol 2016;90(23):10527-34. PMID 27630241
44: Kang JH, Sheu JJ, Lin HC. Increased risk of Guillain-Barre syndrome following recent herpes zoster: a population-based study across Taiwan. Clin Infect Dis 2010;51(5):525. PMID 20642353
45: Kleinschmidt-DeMasters BK, Amlie-Lefond C, Gilden D. The patterns of varicella zoster virus encephalitis. Hum Pathol 1996;27(9):927-38. PMID 8816888
46: Kleinschmidt-DeMasters BK, DeBiasi RL, Tyler KL. Polymerase chain reaction as a diagnostic adjunct in herpesvirus infections of the nervous system. Brain Pathol 2001;11:452-64. PMID 11556691
47: Klompas M, Kulldorff M, Vilk Y, Bialek SR, Harpaz R. Herpes zoster and postherpetic neuralgia surveillance using structured electronic data. Mayo Clin Proc 2011;86(12):1146-53. PMID 21997577
48: Kundratitz K. Experimentelle ubertragung von herpes zoster auf den menschen und die beziehungen von herpes zoster zu varicellen. Monatsschr Kinderheilkd 1925;29:516-22.
49: Lenfant T, L'Honneur AS, Ranque B, et al. Neurological complications of varicella zoster virus reactivation: Prognosis, diagnosis, and treatment of 72 patients with positive PCR in the cerebrospinal fluid. Brain Behav 2022;12(2):e2455. PMID 35040287
50: Leung J, Harpaz R, Baughman AL, et al. Evaluation of laboratory methods for diagnosis of varicella. Clin Infect Dis 2010;51(1):23-32. PMID 20504232
51: Leung J, Harpaz R, Molinari NA, Jumaan A, Zhou F. Herpes zoster incidence among insured persons in the United States, 1993-2006: evaluation of impact of varicella vaccination. Clin Infect Dis 2011;52(3):332-40. PMID 21217180
52: Levin MJ, DeBiasi RL, Bostic V, Schmid DS. Herpes zoster with skin lesions and meningitis caused by 2 different genotypes of the Oka Varicella-zoster virus vaccine. J Infect Dis 2008;198:1444-7. PMID 18826373
53: Liberman AL, Nagel MA, Hurley MC, Caprio FZ, Bernstein RA, Gilden D. Rapid development of 9 cerebral aneurysms in varicella-zoster virus vasculopathy. Neurology 2014;82(23):2139-41. PMID 24827494
54: Lipschultz B. Untersuchungen uber die atiologie der krankheiten der herpesgruppen (Herpes zoster, herpes genitalis, herpes febrilis). Arch Dermatol Syph Orig 1921;136:428-82.
55: Macartney K, McIntyre P. Vaccines for post-exposure prophylaxis against varicella (chickenpox) in children and adults. Cochrane Database Syst Rev 2008;3:CD001833. PMID 18646079
56: Mahalingam R, Wellish M, Wolf W, et al. Latent varicella-zoster viral DNA in human trigeminal and thoracic ganglia. N Engl J Med 1990;323(10):627-31. PMID 2166914
57: Mallick-Searle T, Snodgrass B, Brant JM. Postherpetic neuralgia: epidemiology, pathophysiology, and pain management pharmacology. J Multidiscip Healthc 2016;9:447-54. PMID 27703368
58: Marin M, Zhang JX, Seward JF. Near elimination of varicella deaths in the US after implementation of the vaccination program. Pediatrics 2011;128(2):214-20. PMID 21788222
59: Markus A, Grigoryan S, Sloutskin A, et al. Varicella-zoster virus (VZV) infection of neurons derived from human embryonic stem cells: direct demonstration of axonal infection, transport of VZV, and productive neuronal infection. J Virol 2011;85(13):6220-33. PMID 21525353
60: Matthews E, Beckham JD, Piquet AL, Tyler KL, Chauhan L, Pastula DM. Herpesvirus-associated encephalitis: an update. Curr Trop Med Rep 2022;9(3):92-100. PMID 36186545
61: Mattson SN, Jones KL, Gramling LJ, et al. Neurodevelopmental follow-up of children of women infected with varicella during pregnancy: a prospective study. Pediatr Infect Dis J 2003;22(9):819-23. PMID 14506375
62: Morgello S, Block GA, Price RW, Petito CK. Varicella-zoster virus leukoencephalitis and cerebral vasculopathy. Arch Pathol Lab Med 1988;112:173-7. PMID 3337629
63: Murata K, Miwa H, Kondo T. Polyneuritis cranialis caused by varicella zoster virus in the absence of rash. Neurology 2010;74:85-6. PMID 20038777
64: Nagel MA, Choe A, Traktinskiy I, Cordery-Cotter R, Gilden D, Cohrs RJ. Varicella-zoster virus transcriptome in latently infected human ganglia. J Virol 2011;85(5):2276-87. PMID 21177814
65: Nagel MA, Cohrs RJ, Mahalingam R, et al. The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features. Neurology 2008;70(11):853-60. PMID 18332343
66: Nagel MA, Forghani B, Mahalingam R, et al. The value of detecting anti-VZV IgG antibody in CSF to diagnose VZV vasculopathy. Neurology 2007;68:1069-73.** PMID 17287447
67: Nagel MA, Niemeyer CS, Bubak AN. Central nervous system infections produced by varicella zoster virus. Curr Opin Infect Dis 2020;33(3):273-8. PMID 32332223
68: Nagel MA, White T, Khmeleva N, et al. Analysis of varicella-zoster virus in temporal arteries biopsy positive and negative for giant cell arteritis. JAMA Neurol 2015;72(11):1281-7. PMID 26349037
69: Osler W. The principles and practice of medicine. New York: Appleton, 1892.
70: Oxman MN, Levin MJ, Johnson GR, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med 2005;352(22):2271-84. PMID 15930418
71: Paul R, Singhania P, Hashmi M, Bandyopadhyay R, Banerjee AK. Post chicken pox neurological sequelae: three distinct presentations. J Neurosci Rural Pract 2010;1(2):92-6. PMID 21808511
72: Piquet AL, Cho TA. The clinical approach to encephalitis. Curr Neurol Neurosci Rep 2016;16(5):45. PMID 27021774
73: Piquet AL, Lyons JL. Infectious meningitis and encephalitis. Semin Neurol 2016;36(4):367-72. PMID 27643906
74: Rack AL, Grote V, Streng A, et al. Neurologic varicella complications before routine immunization in Germany. Pediatr Neurol 2010;42(1):40-8. PMID 20004861
75: Reynolds L, Struik S, Nadel S. Neonatal varicella: varicella zoster immunoglobulin (VZIG) does not prevent disease. Arch Dis Child Fetal Neonatal Ed 1999;81(1):F69-70. PMID 10375368
76: Sabry A, Hauk PJ, Jing H, et al. Vaccine strain varicella-zoster virus-induced central nervous system vasculopathy as the presenting feature of DOCK8 deficiency. J Allergy Clin Immunol 2014;133(4):1225-7. PMID 24418481
77: Science M, MacGregor D, Richardson SE, Mahant S, Tran D, Bitnun A. Central nervous system complications of varicella-zoster virus. J Pediatr 2014;165(4):779-85. PMID 25063723
78: Shin E, Chi SA, Chung TY, et al. The associations of herpes simplex virus and varicella zoster virus infection with dementia: a nationwide retrospective cohort study. Alz Res Therapy 2024;16(1):57. PMID 38475873
79: Singh TD, Fugate JE, Rabinstein AA. The spectrum of acute encephalitis: causes, management, and predictors of outcome. Neurology 2015;84(4):359-66. PMID 25540320
80: Skripuletz T, Pars K, Schulte A, et al. Varicella zoster virus infections in neurological patients: a clinical study. BMC Infect Dis 2018;18(1):238. PMID 29801466
81: Steiner P. Zur inokluation der varicellen. Wien Med Wochenschr 1875;25:306.
82: Trujillo-Gomez J, Tsokani S, Arango-Ferreira C, et al. Biofire FilmArray meningitis/encephalitis panel for the aetiological diagnosis of central nervous system infections: a systematic review and diagnostic test accuracy meta-analysis. EClinicalMedicine 2022;44:101275. PMID 35198914
83: Tyring S, Barbarash RA, Nahlik JE, et al. Famiciclovir for the treatment of acute herpes zoster: effects on acute disease and post-herpetic neuralgia. A randomized, double-blind, placebo-controlled trial. Collaborative Famciclovir Herpes Zoster Study Group. Ann Intern Med 1995;123(2):89-96. PMID 7778840
84: Tyzzer EE. The histology of the skin lesions in varicella. Philipp J Sci 1906;1:349-72.
85: Von Bokay J. Uber den aetiologischen zussammenhang der varicellen mit gewissen fallen von herpes zoster. Wien Klin Wochenschr 1909;22:1323-6.
86: Warren-Gash C, Forbes H, Breuer J. Varicella and herpes zoster vaccine development: lessons learned. Expert Rev Vaccines 2017;16(12):1191-201. PMID 29047317
87: Warren-Gash C, Williamson E, Shiekh SI, et al. No evidence that herpes zoster is associated with increased risk of dementia diagnosis. Ann Clin Transl Neurol 2022;9(3):363-74. PMID 35170873
88: Watson CP, Deck JH, Morshed C, Van der Kooy D, Evans RJ. Post-herpetic neuralgia: further post-mortem studies of cases with and without pain. Pain 1991;44:105-17. PMID 1711192
89: Weller TH, Witton HM. The etiologic agents of varicella and herpes zoster: serologic studies with the viruses as propagated in vitro. J Exp Med 1958;108:869-90. PMID 13598817
90: Weller TH, Witton HM, Bell EJ. The etiologic agents of varicella and herpes zoster: isolation, propagation, and cultural characteristics in vitro. J Exp Med 1958;108:843-68. PMID 13598816
91: Whitley RJ. Varicella-zoster virus. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 4th ed. New York: Churchill-Livingston, 1995:1345-51.
92: Yawn BP, Gilden D. The global epidemiology of herpes zoster. Neurology 2013;81(10):928-30. PMID 23999562
93: Yildirim M, Gocmen R, Konuskan B, Parlak S, Yalnizoglu D, Anlar B. Acute cerebellitis or postinfectious cerebellar ataxia? Clinical and imaging features in acute cerebellitis. J Child Neurol 2020;35(6):380-8. PMID 32160830

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Amanda L Piquet MD

Dr. Piquet of the University of Colorado received consulting fees from Alexion/AstraZeneca, EMD Serono, Genentech/Roche, and UCB.
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Editor

John E Greenlee MD

Dr. Greenlee of the University of Utah School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Burk Jubelt MD
Catherine Amlie-Lefond MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Chickenpox (varicella without complication): B01.9

Herpes zoster without complication: B02.9

Postherpetic neuralgia: B02.2
ICD-11: Varicella: 1E90

Varicella without complication: 1E90.0

Zoster: 1E91

Zoster with central nervous system involvement: 1E91.3

Postherpetic polyneuropathy: 1E91.5

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Varicella-zoster virus infections of the nervous system

Associated Disorders

Acute cerebellar ataxia in children
Acute inflammatory demyelinating polyradiculoneuropathy
Reye syndrome

Differential Diagnosis

childhood viral exanthems
radiculopathies
arteritides
encephalitides
herpes simplex
- some arboviruses
- hemorrhagic fevers
- brain abscess (bacterial or fungal)
- toxoplasmosis
- parasitic infection
- Lyme disease
- autoimmune vasculitides

Also Relevant

Acute cerebellar ataxia in children
Acute inflammatory demyelinating polyradiculoneuropathy
Bell palsy
Diagnosis of CNS infections
Herpes zoster oticus
- Molecular diagnosis of CNS infections
- Neuromyelitis optica spectrum disorders
- Painful conditions of the face and head
- Ramsay Hunt syndrome
- Temporal arteritis
- Vaccines for neurologic disorders
- Viral meningitis

VZV infections …

Varicella-zoster virus infections of the nervous system

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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to access the full version.

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Varicella-zoster virus infections of the nervous system

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neuropathies associated with cytomegalovirus infection

Genital herpes: neurologic complications

Neurocysticercosis

Clinical evaluation of peripheral neuropathies

Zika virus: neurologic complications

Gram-negative bacillary meningitis

Monoclonal gammopathy of neurologic significance

Chronic inflammatory demyelinating polyradiculoneuropathy

This is an article preview.
Start a Free Account
to access the full version.