Acute cerebellar ataxia in a 41 year old woman

Moses, Howard; Nagel, Maria A.; Gilden, Donald H.

doi:10.1016/s1474-4422(06)70601-9

Cited by 28 publications

(21 citation statements)

References 17 publications

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“…More recently, proof that VZV can cause serious neurological disease, often in the absence of rash, has been based on serologic analyses to detect VZV-specific antibodies (Shoji et al, 1976), as well as intracellular antigen in patients with zoster meningoencephalitis, cranial and spinal radiculoneuritis (Peters et al, 1979), and intrathecal production of anti-VZV antibodies (Martinez-Martin et al, 1985; Echevarria et al, 1987). Most recently, combined PCR and antibody testing revealed that VZV causes 5% to 27% of all aseptic meningitis (Koskiniemi et al, 2001; Hausfater et al, 2004; Kupila et al, 2006; Frantzidou et al, 2008), which is not altogether surprising because PCR has already shown that VZV causes zoster sine herpete (Gilden et al, 1994), vasculopathy (Gilden et al, 1996), acute (Gilden, 1994) and recurrent (Gilden et al, 2009) myelopathy, acute cerebellar ataxia (Moses et al, 2006; Ratzka et al, 2006), and retinal necrosis (el Azazi et al, 1991; Galindez et al, 1996), all without rash.…”

Section: Discussionmentioning

confidence: 99%

Varicella zoster virus meningitis with hypoglycorrhachia in the absence of rash in an immunocompetent woman

et al. 2009

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We report varicella-zoster virus (VZV) meningitis in a healthy adult woman with no antecedent rash and with hypoglycorrhachia. Cerebrospinal fluid (CSF) examination revealed the presence of VZV DNA, anti-VZV immunoglobulin G (IgG) antibody, and intrathecal production of anti-VZV IgG antibody.Keywords varicella zoster; meningitis; hypoglycorrhachia; PCR; immunocompetent Case reportA 26-year-old healthy Bhutanese woman developed increasing throbbing bitemporal headache with photophobia, severe nausea, and vomiting over 2 days. She had been afebrile and denied neck stiffness. There was no past history of headache, skin rash, recent insect bite, or contact with individuals with infections. She had chickenpox at age 5 years. She had emigrated from Bhutan 7 years earlier, but had not traveled abroad recently. Her sister had been treated for tuberculosis. She worked currently as a nanny; the children under her care were healthy and had received Varivax months earlier. On examination, the patient was afebrile and had no rash, nuchal rigidity, or abnormal neurological signs.On day 6 after becoming ill, white blood cell (WBC) count and routine blood chemistries, liver enzymes, erythrocyte sedimentation rate (ESR), anti-nuclear antibody, rapid plasma reagin, and human immunodeficiency virus testing were negative. Brain magnetic resonance imaging (MRI) revealed an ill-defined T2 hyperintensity in the right frontal lobe, extending from the cortical surface to the frontal horn of the lateral ventricle without mass effect, consistent with a hamartoma or cortical dysplasia. The cerebrospinal fluid (CSF) contained 331 WBCs, 99%

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Section: Discussionmentioning

confidence: 99%

Varicella zoster virus meningitis with hypoglycorrhachia in the absence of rash in an immunocompetent woman

et al. 2009

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“…Cerebellar symptoms present insidiously and progress over months, 3 and cerebellar atrophy can be present on MRI but may well be absent during the early course of PCD. 3 Thus, the absence of cerebellar atrophy does rule out a diagnosis of PCD. However, acute onset and leptomeningeal enhancement on MRI reduced the possibility of PCD in our patient.…”

Section: Discussionmentioning

confidence: 99%

Neoplastic meningitis presenting with acute cerebellar ataxia

Seok¹,

Eun²,

Yoo³

et al. 2011

Journal of Clinical Neuroscience

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“…Like VZV vasculopathy, they also occur in the absence of zoster rash, as demonstrated by reports of VZV meningitis [9], meningoradiculitis [10], and cerebellitis [11], in which diagnosis was confirmed by the detection of VZV DNA or anti-VZV antibody or both in CSF.…”

Section: Neurological Complications Of Vzv Reactivationmentioning

confidence: 97%

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

Gilden

Nagel

Cohrs

et al. 2013

Curr Neurol Neurosci Rep

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Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines, and the virus reactivates to cause zoster (shingles), dermatomal distribution, pain, and rash. Zoster is often followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, vasculopathy, meningoencephalitis, and multiple ocular disorders. This review covers clinical, laboratory, and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system. Additional perspectives are provided by discussions of VZV latency, animal models to study varicella pathogenesis and immunity, and of the value of vaccination of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.

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Acute cerebellar ataxia in a 41 year old woman

Cited by 28 publications

References 17 publications

Varicella zoster virus meningitis with hypoglycorrhachia in the absence of rash in an immunocompetent woman

Varicella zoster virus meningitis with hypoglycorrhachia in the absence of rash in an immunocompetent woman

Neoplastic meningitis presenting with acute cerebellar ataxia

The Variegate Neurological Manifestations of Varicella Zoster Virus Infection

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